Scientific Program

Day 1 :

Keynote Forum

Thomas Boldicke

Helmholtz Centre for Infection Research, Germany

Keynote: Intrabodies knocking down intracellular cancer antigens

Time : 10:00-10:40

Biography:

Biography
Thomas Boldicke has received his PhD in 1982 at the Max Planck Institute of Molecular Genetics, Berlin. He started his carrier as Postdoc at the German Research Centre for Biotechnology (GBF, Brunswick) in the Department of Genetics and Cell Biology by John Collins. Now he is a Senior Scientist at the Helmholtz Centre for Infection Research and Project Leader for intrabodies. In 2011, he qualified as a Professor in Molecular Biology and
Cell Biology at the Technical University of Braunschweig. He is an expert in generating mouse and human hybridomas and in selecting and modifying recombinant antibodies. In the last decade he focused on the construction and characterization of intracellular antibodies. He has published 35 manuscripts.

Abstract:

Intrabodies can be used to target and knock down virtually every protein inside the cell. The knockdown of intracellular cancer antigens by intrabodies is promising. Cancer antigens passing the endoplasmatic reticulum (ER) are inactivated by ER intrabodies retained inside the ER and expressed in the single-chain variable fragment (scFv) format. Cytosolic and nuclear cancer targets are inhibited by neutralizing single domain antibodies which comprises only the variable domain of the heavy chain derived from camels or sharks. This talk will give an overview of in vivo targeting of cancer antigens by intrabodies in mouse tumor models and will demonstrate an example of ER intrabodies inhibiting the polysialyltransferases in rhabdyomasarcoma cells in a xenograft tumor mouse model.

Keynote Forum

Pascal Rihet

Inserm and Aix-Marseille University, France

Keynote: From genome scans to the identification of functional genetic variants associated with malaria resistance

Time : 10:40-11:20

Biography:

Pascal Rihet has a long lasting experience of research in the field of genetics and genomics of infectious diseases. He has mapped malaria and sepsis predisposing genes by using genetic linkage or association approaches. Furthermore, he has identified many variants associated with the disease; most of those genetic variants are located within noncoding regions. He has provided evidence that several variants have a cis-regulatory effect, suggesting that the regulation of gene expression is critical for the pathogenesis. In this way, he has investigated gene expression profiles in patients or in mouse models, and identified a number of genes whose expression is up- or down-regulated before or at the onset of the disease. He was the Deputy Director of the TAGC laboratory. Currently he is the Director of TAGC laboratory. The research scope of the laboratory is Genetics, Genomics and Bioinformatics. He is a Professor of Genomics and Immunology at AMU.

 

Abstract:

The contribution of host genetic factors to resistance or susceptibility to Plasmodium falciparum malaria has been widely studied. Nevertheless, a few genome scans have been performed, and few of them led to the discovery of loci significant at the genome level and to the identification of functional variants potentially causal. Here we describe loci genetically linked to malaria phenotype at the genome level and genetic variants located within those loci and associated with malaria phenotype in two independent populations. Furthermore, we provide evidence of a cis-regulatory effect of the genetic variants, suggesting that those variants are causal. We mainly focus on genes and genetic variants located within chromosome 6p21, which has been linked to mild malaria. These include TNF and NCR3, which encode a major actor of inflammation and a receptor of natural killer cells involved the cytotoxicity function, respectively. Also, the results are in line with those supporting the role of TNF in malaria on the one hand and allow us to propose a new biological model to explain the association of a cis-regulatory variant of NCR3 with mild malaria, on the other hand. Also, the genetic variation that alters the activation of natural killer cells may influence human malaria resistance. 

Day 2 :

Keynote Forum

Huang Wei Ling

Medical Acupuncture and Pain Management Clinic, Brazil

Keynote: Why do patients still catch hospital infections despite the practice of infection prevention and control programs?

Time : 10:00-10:40

Biography:

Huang Wei Ling has graduated in Medicine in Brazil, specializing in infectious and parasitic diseases, a General Practitioner and Parenteral and Enteral Medical Nutrition Therapist. Once in charge of the Hospital Infection Control Service
of the City of Franca’s General Hospital, she was responsible for the control of all prescribed antimicrobial medication, and received an award for the best paper presented at the Brazilian Hospital infection Control Congress in 1998. She was coordinator of both the Infection Control and the Nutritional Support Committee in Sao Joaquim Hospital in Franca, and also worked at the infectious Sexually Transmitted Disease Reference Center. She is the owner of the
Medical Acupuncture and Pain Management Clinic, and since 1997 she has been presenting her work worldwide concerning the treatment of various diseases using techniques based on several medical traditions around the world.

Abstract:

Statement of the Problem: Very few publications provide sound scientific data used to determine which components are essential for infection prevention and control (IPC) programs in terms of effectiveness in reducing the risk of infection. In recent years, a range of regional best practice or policy principles have been developed that address what could be considered as core components of IPC programs. However there remains a major gap in relation to the availability of international best practice principles for core components of IPC programs.

Purpose: The purpose of this study was to show why patients still catch hospital infections despite IPC programs. A better understanding of a variety of theories is needed that could explain the physiopathology of diverse diseases described in the medical past history, which are usually disregarded clinically today. A broader view seems to show the necessity of seeing the patientas a whole; not only focusing on the disease in the prevention of these hospital infections.

Methodology: A review of these theories such as those presented by Hippocrates (Natural forces within us are the true healers of disease), as well as others from oriental medicine, which explain that diseases originate from three factors: external (exposure to cold, heat, humidity, wind and dryness), internal (emotional) and dietary.

Findings: Having a broader view of the patient as a whole (Yin, Yang, Qi, blood energy and heat retention), we can understand better the formation of hospital infection which is a systemic energy reaction of our body undergoing normal hospital treatment.

Conclusion: To understand better why a patient is still catching hospital infections, despite these IPC programs, we need to broaden our view observing all emotional, environmental and dietary factors, as well as studying the patient’s energy situation atthe moment of admittance identifying the risk of hospital infection.

 

Keynote Forum

Thomas Grundstrom

Umeå University, Sweden

Keynote: Regulation of diversification and affinity maturation of antibodies

Time : 10:40-11:20

Biography:

Thomas Grundström has completed his Doctorate at Umeå University in 1981 and his Medical degree in 1982. He was a Postdoc during 1982-1984 in the laboratory of Professor Pierre Chambon, Institut de Chimie Biologique, Strasbourg, France, where he characterized the first discovered enhancer of transcription. He is a Professor at the Department of Molecular Biology at Umeå University since 1994. He has been studying Ca2+ sensor proteins and eukaryotic transcription and discovered the first direct Ca2+/calmodulin inhibition of a transcription factor. He has characterized the Ca2+ regulation of many transcription factors and other regulatory proteins with a main focus on the immune system. He is presently studying regulation of production of antibodies. He studies how somatic hypermutation (SH) and class switch recombination (CSR) are targeted and the regulation of the protein complex that performs SH and CSR.

Abstract:

B-lymphocytes can modify their immunoglobulin (Ig) genes to generate antibodies with a new isotype and enhanced affinity. Activation-induced cytidine deaminase (AID) is the key mutagenic enzyme that initiates these processes. How somatic hypermutation (SH) and class switch recombination (CSR) are targeted and regulated to understand how we achieve good antibodies. The trans-acting factors mediating specific targeting of AID and thereby SH and CSR have remained elusive. How AID is recruited was still a big mystery. We show that mutant E2A transcription factor with defect inhibition by the Ca2+ sensor protein calmodulin results in reduced B cell receptor (BCR), IL4- plus CD40 ligand-stimulated CSR to IgE. AID is shown to be together with the transcription factors E2A, PAX5 and IRF4 in a complex on key sequences of the Igh locus in activated mouse splenic B cells. Calmodulin shows proximity with them after BCR stimulation. Direct protein-protein interactions are shown to enable formation of the complex. BCR signaling reduces binding of the proteins to some of the target sites on the Igh locus, and calmodulin resistance of E2A blocks this reduction. Thus, E2A, AID, PAX5 and IRF4 are components of a CSR and SH complex that calmodulin binding redistributes on the Igh locus. We present also that initiation of antibody diversification leads to formation of a mutasome, a complex between many proteins that enable repair at high error rate of the uracils made by AID on Ig genes but not on most other genes. We show also that BCR activation, which signals end of successful SH, reduces interactions between some proteins in the complex and increases other interactions in the complex with varying kinetics. Furthermore, we show increased localization of SH and CSR coupled proteins on switch regions of the Igh locus upon SH/CSR and that BCR signaling differentially change the localization.

 

Biography:

Sasha Berdichevski is a Post-doctoral Research Associate in Engineering De­partment at University of Cambridge, UK. She has obtained a Blavatnik Fel­lowship by the Blavatnik Family Foundation, British Council and University of Cambridge, and currently she holds a Marie Curie Fellowship. She has been awarded as outstanding Researcher in Engineering and Science Award and Prize for Excellence in Nano-science and Nanotechnology during her PhD in the Technion, Israel. She has published her research in leading journal papers, and co-authored publications in three books. Her research interests include “Biomaterials, tissue engineering, scaffold-tissue/cell interactions, and scaf­folds’ 3D geometry function relationship”.

 

Abstract:

One of the main goals in producing engineered tissues at clinically relevant dimensions is creating perusable vascular networks, since cell viability and function cannot be sustained through diffusion alone. Therefore a great deal of research in the field of regenerative medicine has been devoted to establish in vitro pre-vascularization approaches. In this context, we propose to create capillary-like networks using human umbilical cord endothelial cells, cultured with human osteoblasts, as these cells were demonstrated to have both direct and indirect pro-vasculogenic effects, within freeze-dried collagen scaffolds with tailored pore architecture. We guided scaffold pore architecture by manipulation of the freeze-drying conditions; producing porous scaffolds with randomly oriented (isotropic) or uniaxially aligned (anisotropic) pore architectures. We characterized the scaffolds’ structural, permeability and mechanical properties and showed that pore architecture affected the invasion, morphology and self-organization of the endothelial cells, in both mono- and co-cultures. Results showed that cell proliferation and metabolic activity were affected by pore architecture as well. Pore anisotropy promoted more uniform cell infiltration deeper within the scaffold, and improved cell organization into multi-cellular vessel-like networks. Co-culture conditions further improved the network quality. We suggest that deeper cell infiltration, along with more efficient medium perfusion within the anisotropic scaffolds account for these findings. However, the exact mechanism and conditions for optimal 3D vascular network formation as function of pore architecture have yet to be established.

 

Keynote Forum

Roman Bauer

Newcastle University, UK

Keynote: Computational modelling of neural tissue growth

Time : 12:20-13:00

Biography:

Roman Bauer is an MRC Research Fellow at Institute of Neuroscience-Newcastle University, with joint affiliation with the School of Computing. His research involves computational models to better understand how neural tissue evolves during development. He received his Bachelor’s and Master’s Degree in Computational Science and Engineering from ETH Zurich, Switzerland. Afterwards, he did his Doctoral studies at Institute for Neuroinformatics (INI)- ETH and University Zurich, working on simulations of cortical development. After Postdoctoral work at Newcastle University from 2013 to 2016, he took up a prestigious MRC fellowship. His research interests include “Neural development, neural degeneration, neural disorders, gene regulatory networks and cryopreservation”.

 

Abstract:

Biological tissue often exhibits extraordinary complexity. For example, neural tissue comprises large numbers of neurons with cell-type specific axonal and dendritic arborisation, highly structured synaptic connectivity, and fine-tuned electrical activity. A better understanding of how such tissue complexity develops is often essential for tissue engineering purposes. To this end, author will present some of his computational models of neural tissue development, demonstrating how complex structure and function can be generated based solely on simple genetic rules. These multi-scale models comprise intracellular as well as extracellular dynamics in a detailed, physical 3D environment. In particular, author will elaborate on computational models of cortical and retinal structure and function, ranging across different spatial scales. By modelling the biological self-organization of such tissue, predictions are made and so novel hypotheses are generated, which can be experimentally validated. Moreover, these models can inform and guide tissue engineering protocols. Finally, author will discuss modern computational approaches, including the BioDynamo software, which is a collaborative project with project partner CERN Openlab. Overall, author will emphasize the importance of computer models as a tool to advance tissue engineering approaches.

 

Location: Spessart

Session Introduction

Armin Laboratories

Germany

Title: Exhibitor
Biography:

Armin Schwarzbach, MD PhD has been at the forefront of diagnostic testing and tick-borne research for more than 20 years, and his expertise in diagnosing and treating infectious diseases is second to none having tested over 20,000 patients. He was a Board Member of the International Lyme and Associated Diseases Society (ILADS), is an Advisory Board member of AON M London, and serves as an expert on advisory committees on Lyme Disease in Australia, Ireland, France and Germany. Dr. Schwarzbach is a Board Member of the German Borreliosis Society. Being acutely aware of the insufficient, sensitivity and standardisation of Borrelia antibody ELISA and immunoblot tests, Dr. Schwarzbach offers tests with greater sensitivity and specificity. His new laboratory is in operation since 2015.

Abstract:

As infections with Borrelia are often accompanied by coinfections, they should also be taken into consideration. coinfections complicate the diagnosis and treatment because they often evoke a more complex symptomatology. The co-pathogens can cause very specifi c, but also unspecifi c and “overlapping” symptoms. in order to better detect these pathogens, Dr. schwarzbach has developed a coinfections checklist. The analysis of the checklist enables a better targeted selection of necessary laboratory tests for coinfections. This preselection prevents expensive panel testing for our patients. our team will gladly provide you with the automated coinfections checklist and more information about our modern diagnostic test methods.

 

Nisco Engineering

Switzerland

Title: Exhibitor
Biography:

Abstract:

Nisco Electrostatic Units VarV1 and VAR Jet2Go
An excellent method of production for small alginate beads containing living cells or other biological materials in a controllable manner is the use of an electrostatic bead generator. The basic principle of the instrument is the application of an electrostatic force to pull droplets from a needle tip into a gelling bath. The Nisco instrument VARV1 is designed for research and production of small quantities of spherical alginate beads ranging in size from 200 to 2400 μm. The bead generator VARV1 has been used successfully in several studies involving immobilization of living cells in the field of stem cell research, 3D cellular models, controlled release, tissue engineering and regenerative medicine. The production of different high quality threads is possible with use of our VARJet2Go units, standard modular electrospinning devices. The production of core-shell threads with use of our superior coaxial nozzles with wide range of diameters is possible as well.

 

Chemometec

Denmark

Title: Exhibitor
Biography:

Founded in 1997, Chemometec specialises in the design, development and production of high quality instruments using patented technology for a wide range of applications in cell counting and evaluation. Like many companies with unique technology, we had an interesting birth as talented development specialists with new ideas broke free from conservative corporate constraints.We work closely with life science companies, research institutes, universities, hospitals, specialist clinics and a wide range of food and beverage manufacturers, matching our technical development expertise to customer needs - with quality results, reliability, cost-efficiency and ease-of-operation as our guiding principles. We support a growing customer base worldwide with responsive technical services and the ready availability of a wide range of consumables. 

 

Abstract:

The NucleoCounter® NC-200™
One step viability and cell count
Fast, precise and objective one step viability and cell count with only one cassette. Simply fill the cassette, load it, and press “RUN”. In less than 50 seconds you will have fast, precise and objective results. The NucleoCounter® is the most precise cell counter in the life science market. It uses the disposable Via1-Cassette™ to combine cell sampling, staining, loading and counting into a single workflow to maximize precision and eliminate human error. Simply insert the tip of the cassette into your cell sample and press the plunger to load your cells.

  • Classical Immunology | Tissue Engineering and Regeneration | Immunoinformatics | Immunological Disorders | Autoimmune Diseases | Infectious Disease Drivers | Emerging and Re-emerging Infectious Diseases | Remedy for Immunity and Infection
Location: Spessart

Chair

Hadaf Dhafir Al Yaseen

University of Baghdad, Iraq

Co-Chair

Yawei Liu

University of Copenhagen, Denmark

Biography:

She holds a BSc. in microbiology and PhD in immunology and has about 17
years of research experience in infectious diseases and vaccines. Her research
path started as research assistant at Pasteur Institute of Iran, where she was involved in recombinant vaccine studies against Leishmania major, and assisted the group leader to establish and run the “Molecular Immunology and Vaccine lab”. She fulfilled her PhD studies at Stockholm University on the general topic of “Human genetic factors involved in immunity to malaria”,while contributing to allergy studies as well. As Postdoctoral researcherand Assistant Professor her research focus turned towards genetic diversityof malaria parasite in relation to transmission intensity and prospective studies of malaria in travelers. Years of engagement with tropical diseases provided her with experience of filed study as well as broad collaborative network. Beside  academic education, she schooled for ICH-GCP, Pharmacovigilance-Drug Safety, GMP, and coaching-leadership.

Abstract:

The rapid clearance of malaria parasite DNA from circulation has widely been accepted as a fact without being systemically investigated. In this longitudinal study, we examined the duration of PCR positivity as well as the presence of gametocytes in adult travelers treated for Plasmodium falciparum malaria in a malaria-free setting, using microscopy, species-specific qPCR, merozoite surface protein 2 (msp2)-genotyping PCR, and gametocyte-specific qPCR. Venous blood was collected at the time of admission and prospectively up to one year. Patients were treated with a full regimen of six doses of artemether-lumefantrine (AL). In 31 successfully treated individuals, asexual parasites were seen by microscopy until two days after treatment, whereas parasite DNA was detected by msp2- and species-specific PCR up to days 31 and 42, respectively. Statistical modelling predicted 26% (± 0•05 SE) species-specific PCR positivity until day 40 and estimated 48 days for all samples to become PCR negative. Gametocytes were detected by microscopy and PCR latest two days after treatment. CT values correlated well with microscopy-defined parasite densities before but not after treatment started. Duration of PCR positivity was correlated neither with the initial (asexual) parasite densities nor with the initial presence of gametocytes.These results reveal that PCR positivity can persist several weeks after treatment without evidence of viable sexual or asexual parasites, and that the removal of dead parasites and their debris is not as rapid as it is believed, indicating that PCR may overestimate post-treatment parasite prevalence in epidemiological studies, and underestimate drug efficiency in clinical management and trials. This report underlines an important diagnostic matter essentially in infectious diseases and particularly in malaria, and points out the need for detection tool as sensitive as PCR and as accurate as microscopy.

Biography:

Hans Kollberg is Professor emeritus, Pediatrics, Children´s University Hospital,Uppsala. He has a Specialization in Pediatrics from Swedish Medical
Board in 1966. He holds a Medical Doctors Degree (MD) in Pediatrics from Uppsala University, Sweden 1961. He started his career as Staff Physician, Good Samaritan Hospital, Phoenix, Arizona during 1959-1966. He extended his service as a Director of the CF Center, University Hospital, Uppsala in 1968-1982 and Umea in 1985-1999. He was Professor at the University of Kuwait during 1982-1985. He has been a recipient of many awards and grants. He is the Founder of the Swedish Cystic Fibrosis Association. His research experience includes various programs, contributions and participation in different countries for diverse fields of study. His research interests as a Research Scholar reflect in his wide range of publications in various national and international journals.

Abstract:

There is an increasing prevalence of antibiotic resistant bacteria. This makes traditional antibiotics less effective. More than 25000 people in Europe die each year from infections of resistant bacteria. This emphasizes the need to find alternatives to antibiotics. The drug should fight infections, it should not give resistant bacteria or viruses, it should be easy to scale up and it should be cheap. Such a drug exists. Avian antibodies from immunized hens act as strong weapons against a series of common infections. Hence these can be used either as a complement or an alternative to antibiotics. It is high time for health authorities, pharmaceutical companies, physicians, and researchers etc., to be involved in the fight against infectious diseases by joining this strong pull for avian antibodies-IgY. Clinical studies are carried out including use of IgY will diminish the development of antibiotic resistant microbes.

  • Lunch Break
Location: @ Rastaurant palate friend

Session Introduction

Huang Wei Ling

Medical Acupuncture and Pain Management Clinic, Brazil

Title: Can recurrent furunculosis be treated without the use of antibiotics?
Biography:

Huang Wei Ling has graduated in Medicine in Brazil, specializing in infectious
and parasitic diseases, a General Practitioner and Parenteral and Enteral Medical Nutrition Therapist. She was in charge of the Hospital Infection Control Service of the City of Franca’s General Hospital, she was responsible for the control of all prescribed antimicrobial medication, and received an award for the best paper presented at the Brazilian Hospital infection Control Congress in 1998. She was coordinator of both the Infection Control and the Nutritional Support Committee in Sao Joaquim Hospital in Franca, and also worked at the infectious Sexually Transmitted Disease Reference Center. She is the owner of the Medical Acupuncture and Pain Management Clinic, and since 1997 she has been presenting her work worldwide concerning the treatment of various diseases using techniques based on several medical traditions around the world.

Abstract:

Background: Furunculosis is a deep infection of the hair follicle leading to abscess formation with accumulation of pus and necrotic tissue. Furuncles appear as red, swollen, and tender nodules on hair-bearing parts of the body, and the most common infectious agent is Staphylococcus aureus, but other bacteria may also be causative. The management of recurrent furunculosis is problematic and may be disappointing. Simple incision and drainage may be sufficient in solitary lesions, but systemic antibiotic therapy may be required. S. aureus has the ability of developing resistance to different antibiotics. Traditional Chinese Medicine (TCM) believes furunculosis is mostly caused by invasion of dampness and heat. The treatment in TCM is intended to dissipate heat and detoxify the body.
Purpose: The purpose of this study is to demonstrate that recurrent furunculosis can be treated without the use of antibiotics.
Methods: Through the report of two clinical cases, both men, suffering from recurrent furunculosis, presented little improvement with the use of antibiotic therapy. Through earlier medicine theories, such as TCM, methods for energy balance of yin, yang, qi and blood were used, allied with apex ear bloodletting to withdrawal of internal heat, as well as dietary counseling.
Results: Both cases obtained a significant improvement with dietary counseling according to TCM and auricular acupuncture sessions associated with apex ear bloodletting to clear out the internal heat.
Conclusion: By reporting these two clinical cases, we can conclude that recurrent furunculosis can be treated without the use of antibiotics. For this goal, we must resort to earlier medicine theories like TCM to treat the root of the problem, not only the symptom.

Biography:

Desheng Hu has received his PhD degree in Immunology at the Leibniz Institute for Ageing Research, Jena University, Germany in 2012. After that he did his Postdoc training in the Institute for Immunology of Helmholtz Zentrum Munich and in the Institute for Immunology of Ludwig Maximilian University of Munich. In 2017, he went back to China and established his own research group in Wuhan Union Hospital, Wuhan, China. His research focuses on Vascular Immunology. So far, he has published several papers in high impact factor journals, such as Nature Immunology, Immunity and Circulation Research.

Abstract:

Tertiary lymphoid organs (TLOs) emerge during non-resolving peripheral inflammation, but their impact on disease progression remains unknown. We have found in aged Apoe-/- mice that artery TLOs (ATLOs) controlled highly territorialized aorta T cell responses. ATLOs promoted T cell recruitment, primed CD4+ T cells, generated CD4+ , CD8+ , T regulatory (Treg) effector and central memory cells, converted naive CD4+ T cells into induced Treg cells, and presented antigen by an unusual set of dendritic cells and B cells. Meanwhile, vascular smooth muscle cell lymphotoxin β receptors (VSMC-LTβRs) protected against atherosclerosis by maintaining structure, cellularity, and size of ATLOs though VSMC-LTβRs did not affect secondary lymphoid organs. Atherosclerosis was markedly exacerbated in Apoe- /- Ltbr-/- and to a similar extent in aged Apoe-/-Ltbrfl/fl, Tagln-cre mice. These data support the conclusion that the immune system employs ATLOs to organize aorta T cell homeostasis during aging and that VSMC-LTβRs participate in atherosclerosis protection via ATLOs.

Rochelle Van der Merwe

South African Society of Travel Medicine, South Africa

Title: The Hysteria surrounding Listeria in South Africa
Biography:

Rochelle is a registered medical practitioner, completed her studies in 2010
at the University of Pretoria. She finished her Diploma in Emergency Medicine
in 2017 along with her certificate in Travel Medicine in 2016. She accomplished her dispensing license and have been updated with ATLS, ACLS and PALS in South Africa. She works for one of the busiest, private hospital, Emergency departments in South Africa seeing a multitude of trauma and medical emergencies. She is interested in Family and Travel Medicine practice affiliated with the ED with a special interest in Aesthetic Medicine. She is currently serving on the executive board for the Society of Travel Medicine in South Africa working closely with the NICD with all infectious disease monitoring in SA and submitting interesting case studies to Federation of
Infectious Diseases in SA (FIDSSA) on behalf of SASTM.

Abstract:

Listeriosis is the new and deadly disease emerging after years of being the quiet one sitting in the corner while HIV and Malaria caused havoc and massive outbreaks and mortality rates sky rocketing. Our population is well informed and up to date on most of the diseases and as soon as listeria was mentioned in the same sentence as processed foods, we created mass hysteria in all the emergency departments with worried patients, ill-informed patients and really sick patients, with very little knowledge about listeria. I want to discuss the
pathogenicity as a re-emerging disease we have not heard from in a long time with very little information regarding pandemic and epidemics. Being in the midst of the hysteria, I think giving an inside view and up close, first-hand experience on what happened as soon as the outbreak was confirmed leading up to the massive explosion of patients literally running to ED after the source was confirmed as one of our leading manufacturers and producers of processed meat. We have had around 180 deaths in SA due to Listeria especially in the age groups of the very young, elderly, pregnant and immunosuppressed patients. The biggest factor leading to the outbreak initially was that we were not looking for it as we were so focused on Malaria as leading cause of fever and confusion etc. at the time of the outbreak and NICD confirmed that Malaria deaths doubled in 2017 vs. 2016. Listeriosis was monitored and regarded as a minor infection, but, while everyone was focused on travel history, Listeria was silently killing dozens. I would like to include the basic information as to what, where and how as the simple things were missed while we were looking for complicated illnesses

Biography:

J Di Cristofaro has her experience in Human Genetics applied to Personal Medicine. She graduated PhD in Oncology from the Aix Marseille University, Immunological Therapies in Paris Descartes University and Forensics in Bordeaux University. After completing her PhD at INSERM, she has joined the French Blood Center to set up a genetic analysis platform dedicated to Immunogenetics, Immunohematology and Anthropogenetics. She has worked on molecular carcinogenesis and set up markers to help carcinomas classification and worked in anthropogenetics on Y chromosome phylogeny. Her current researches focus is HLA Ib molecules in immunization and inflammatory responses. Her aim is to validate inflammatory and/or alloimmunization prognostic markers in blood transfusions, pregnancies, transplantation or inflammatory diseases. Her team works on genetic polymorphisms, transcriptional expression variation both at qualitative level and quantitative level, protein expression and function.

Abstract:

Today topic is human leukocyte antigen (HLA) non-classical class Ib genes, HLA-G, -E and -F, involved in immune tolerance. HLA-G immune-inhibitory role acting directly on immune cells is extensively documented. HLA-G inhibits natural killer (NK) cytotoxicity. This molecule is also able to negatively influence antigen presentation of dendritic cells (DC), B and T lymphocytes activation and proliferation. HLA-G gene is characterized by few coding alleles and polymorphic regulatory regions, organized in a restricted number of haplotypes (UTR). Both HLA-G genetic polymorphism and expression are correlated to clinical outcome in different pathologies, particularly in inflammatory disease and organ transplantation. HLA-G phylogeny reflects HLA-G haplotype specific association with different clinical conditions. HLA-G sequences associated with immune impairments in pathological conditions are grouped in same phylogenetic clades. Furthermore, this molecule displays several isoforms, soluble or membrane bound, generated by alternative splicing. Besides its expression in immune cells, HLA-G is expressed by the epithelium and is implicated in cell proliferation and differentiation. However, little is known about the qualitative and quantitative HLA-G expression in epithelial cells. HLA-E gene is the least polymorphic of the HLA class Ib genes. While its transcripts have been detected in several tissues, membrane expression appears to be limited in physiological condition to endothelial cells, T and B lymphocytes, macrophages and trophoblast cells. HLA-E peptide-binding groove, composed by α1 and α2 domains, loads highly conserved peptides mainly derived from classical HLA class I leader peptide sequences. HLA-E binds preferentially HLA-G signal peptide. HLA-E inhibit
NK cytotoxicity trough the CD94/NKG2A inhibitory receptor. HLA-F appears to be expressed mostly in intracellular compartment; its surface expression is detected on activated B, T, and NK cells in vitro and on extravillous trophoblast that had invaded the maternal decidua in vivo. HLA-F, expressed as an open conformer molecule, binds the inhibitory receptor KIR3DS1.

  • Networking & Refreshment Break
Location: @ Foyer
Biography:

Prof. Dr. Hadaf Dhafir Al Yaseen was faculty in University of Baghdad in the
Department of Biochemistry, College of Medicine at University of Baghdad. She finished her Post Doctorate in Clinical Biochemistry at Al-Nahrain University. She is currently the head of the Department of Clinical Biochemistry, University of Baghdad, Iraq. She actively participated in 43 local conferences in Iraq and 26 abroad, making a total of 69 conferences attendance and paper presentation. She also published 85 articles.

Abstract:

Hepatitis C virus (HCV) is a serious infectious disease that can cause lifelong infection. Infection with chronic hepatitis C virus (HCV) can lead to autoimmune hepatitis (AIH) in a minority of patients. Viral infection induces, both (in vivo and in vitro) tumor necrosis factor (TNF-alpha) production in hepatocytes, and these findings suggest that TNF-alpha may have an important role in human liver diseases induced by viruses, together with the prolactin hormone, which is an endocrinal hormone that acts like a cytokine involved in immune response. Our study showed that chronic hepatitis C virus infection associated with a statistical significant increase in the antismooth muscle antibody, while no statistical significant increase in antinuclear antibody were shown in this study. The study elucidated a statistically non-significant increase in mean value of prolactin hormone in chronic hepatitis C patients but a  significant increase in tumor necrosis factor-alpha. No significant correlations were found between prolactin hormone and tumor necrosis factor-alpha. The study concluded that chronic hepatitis C associated with an immunological abnormality mainly represented with antismooth muscle antibody. Tumor necrosis factor-alpha increased in chronic hepatitis C virus infection with no significant correlations with prolactin hormone.

Biography:

Yawei Liu has a medical doctor background and has been doing medical research for more than 10 years. Since her Ph.D., she mainly focused on the role of neurons in the regulation of auto-reactive T cells and central nervous system (CNS) inflammation. We reported a novel function for neurons as being highly immune-competent cells, based on their crucial role in the regulation of T-cell responses and CNS inflammation in models of multiple sclerosis

Abstract:

Neurons reprogram encephalitogenic T cells (T(enc)) to become regulatory Treg cells FoxP3+Tregs or FoxA1+Tregs. We reported previously that neuronal ability to generate FoxA1+Tregs was central to preventing neuroinflammation in experimental autoimmune encephalomyelitis (EAE). Mice lacking the cytokine interferon (IFN)β were defective in generating FoxA1+Tregs in the brain. Neuron-induced FoxA1+Tregs were capable of preventing chronic and demyelinating EAE in mice lacking IFNβ. Here we show that lack of neuronal IFNβ- signaling was associated with lack of neuronal expression of program death-ligand1 (PDL1), which also prevented their ability to reprogram Tenc cells to FoxA1+Tregs. Transfer of IFNβ competent encephalitogenic T cells to mice lacking IFNβ or its receptor; IFN AR in the brain (NesCre:Ifnarfl/fl) led to the absence of FoxA1+Tregs generation and aggravated neuroinflammation. We identified that IFNβ activated neuronal PI3K/Akt signaling. Phosphorylated Akt consequently bound to transcription factor FoxA1, which upon translocation to the nucleus induced neuronal PDL1 expression. Conversely, inhibition of PI3K/Akt, or FoxA1 and PDL1 knock-down blocked neuronal ability to generate FoxA1+Tregs. Our study identified crucial molecular player’s central for neuronal ability to reprogram pathogenic T-cells and to generate FoxA1+Tregs, which could be a therapeutic target to prevent neuroinflammation.

Biography:

Sameh Elmorsy Hassan has an experience in Neurosurgery for nine years in educational hospitals, currently pursuing his MD of Neurosurgery in Cairo University. He has completed his MSc in Neurosurgery. He is a Member of ESA, SPINE, Member of ESNS a lot of conferences about Neurosurgery and Spine Administrator of Egyptian and World Neurosurgeons Community on telegram.

Abstract:

Discitis accounts for nearly 2.2 of 100,000 populations and its presence is an indicator for immunocompromisation, as its risk factors includes diabetes mellitus, IV drug abuse and hemodialysis. As disc nutrition is through diffusion from end plates. So once you diagnose discitis you have to search for immunocompromized agent asking for lab is mandatory to manage medically is the best choice, unless there is refractory pain or neurological deficits, following up of patient by erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) first sign of improvement is decrease of CRP it occurs in two weeks. In acute stage of inflammation surgical intervention is not recommended but in chronic stage you can manage it surgically. Discitis is a serious problem which may cause death and it’s a vicious circle as risk factors are immunocompromization and results are more compromising most probably septicaemia or viraemia is the cause of death.Most appropriate antibiotics should be selected for 3-6 months; intradiscal injection of antibiotics may decrease postoperative discitis as proved by meta-analysis. How discitis happen, risk factors, medical treatment, surgical, what to choose when you choose.

  • Clinical Immunology | Tissue Engineering and Regeneration | Immunological Variability | Immunity and Host defence | Immune Adverse Effects | Microbiology and Clinical Infections | Versatile Immunology | Study of Evolution
Location: Spessart

Chair

Hans Kollberg

Uppsala Universitet, Sweden

Co-Chair

Manijeh Vafa Hofmann

Karolinska Institute, Sweden