Day 1 :
Keynote Forum
Giulio Tarro
Foundation de Beaumont Bonelli for Cancer Research, Italy
Keynote: Tumor liberated protein (TLP) as potential vaccine for lung cancer patients
Time : 10:00-10:35
Biography:
Giulio Tarro graduated from Medicine School, Naples University (1962). He has been a Research Associate, Division of Virology and Cancer Research, Children’s Hospital (1965-1968); Assistant Professor of Research Pediatrics, College Medicine (1968-1969), Cincinnati University, Ohio, USA; Oncological Virology Professor, Naples University (1972-1985). Chief Division Virology (1973-2003). He was the Head of the Department Diagnostic Laboratories for the period 2003-2006. He was the Emeritus for D Cotugno Hospital for Infectious Diseases, Naples in 2006. Since 2007 he has been the Chairman of Committee of Biotechnologies and VirusSphere, World Academy Biomedical Technologies, UNESCO, Adjunct Professor Department Biology, Temple University, College of Science and Technology, Philadelphia. He is a Recipient of the Sbarro Health Research Organization Lifetime Achievement Award (2010). His researches have been concerned with the characterization of specific virus-induced tumour antigens, which were the "finger-prints" left behind in human cancer. His achievements include patents in field: discovery of respiratory syncytial virus in infant deaths in Naples and of tumour liberated protein as a tumour associated antigen, 55 kilodalton protein overexpressed in lung tumours and other epithelial adenocarcinomas.
Abstract:
Tumor liberated protein (TLP) has been previously described as a TAA (complex) present in the sera from lung cancer patients with early stage disease. Since early detection improves overall survival in lung cancer, identification of screening biomarkers for patients at risk for the development of this disease represents an important target. Starting from the peptide epitope RTNKEASI previously isolated from TLP complexes, we generated a rabbit anti-RTNKEASI serum. This antiserum detected and immunoprecipitated a 55kDa protein band in the lysate of the lung cancer cell line A549. This protein band was identified as aldehyde dehydrogenase isoform 1A1 through mass spectrometry, revealing the molecular nature of at least one component of the previously described TLP complex. Next, we screened a cohort of 29 lung cancer patients (all histologies), 17 patients with non-neoplastic lung pathologies and 9 healthy donors for the presence of serum ALDH1A1 and global serum ALDH by enzyme-linked immunosorbent assay. This analysis indicated that the presence of ALDH was highly restricted to patients with lung cancer. Interestingly, the global ALDH test detected more lung cancer patients compared to the ALDH1A1-specific test, suggesting that other ALDH isoforms might add to the sensitivity of the assay. Our data suggests that ALDH levels may therefore be evaluated as part of a marker panel for lung cancer screening. Finally, the ability of the immune system to recognize a TAA, enables the development of a vaccine approach for preventive and therapeutic application and represents a main target of this field of research.
Keynote Forum
Gilbert Glady
European Bio Immun(G)en Medicine Association, France
Keynote: Small or large the non-coding RNAs maintain order in the genome world and therefore can be used for a therapeutic aim
Time : 10:35-11:10
Biography:
Gilbert Glady acquired expertise in Immunology and Immunogenetics, and also developed interest for Alternative Medicines during the last twenty years that lead him to Nanomedicine and Nanobiotechnology. He became the creator of the BI(G)MED method (Bio Immune(G)ene Medicine) and Director of EBMA, the European association for training the medical profession in BI(G)MED in 2010. He has participated in numerous international congresses in the field of Immuno-Allergology, Infectiology and Oncology with posters and oral presentations.
Abstract:
In mammalian cells, the vast majority of transcribed RNAs are noncoding. Many of them are processed to generate small RNAs, including microRNAs, the best-known class of small RNAs. Other transcripts, so- called long noncoding RNAs or lncRNAs, remain larger than 200 nucleotides in their mature form. Through their interaction with DNA, RNA, and proteins, ncRNAs affect all levels of gene regulation, including chromatin remodeling, transcription, pre-mRNA splicing, mRNA turnover, mRNA translation, and protein stability. Through this multi-leveled influence on protein expression patterns, these vast families of noncoding RNAs affect all aspects of cell metabolism, including cell division, senescence, differentiation, stress response, immune activation, and apoptosis. It has recently become apparent that it exists a mutual regulatory influence between microRNAs and lncRNAs. A number of studies over the past decade have also begun to uncover the interaction among mammalian lncRNAs and miRNAs. (1) LncRNAs are targeted by miRNAs to reduce lncRNA stability. (2) LncRNAs can also function as molecular decoys or sponges of microRNAs, reported in a few circular RNAs studies. In addition, (3) lncRNAs can also compete with miRNAs for binding to shared target mRNAs and (4) are precursors for the generation of miRNAs to silence target mRNAs. All these mechanisms will directly alter the cellular response in physiologic and pathologic processes, making them therapeutic targets of great interest. A nanobiotechnology-based method, called Bio Immune (G)en Medicine, has dared to take up the challenge and uses these interactions between non-coding RNAs to regulate gene expression in a large number of pathologies exhibiting significant deregulation at the immuno-genetic level. Some clinical examples, in particular in oncology, will illustrate the method and facilitate its understanding.
Keynote Forum
Moiz Bakhiet
Arabian Gulf University, Bahrain
Keynote: Interleukin 1 receptor antagonist and 2'-5' oligoadenylate synthetase-like molecules as novel biomarkers for multiple sclerosis patients
Time : 11:30-12:05
Biography:
Moiz Bakhiet, Professor of Immunology, is the CEO (Founder) of Princess Al-Jawhara Center for Molecular Medicine, Genetics and Inherited Diseases. He is a Professor and Chairman of the Department of Molecular Medicine, College of Medicine and Medical Sciences, Arabian Gulf University and is a senior Consultant Neurologist at the Arabian Gulf University, Kingdom of Bahrain. Professor Bakhiet received his M.B.B.S. from the Faculty of Medicine, University of Khartoum and his Ph.D. in Medical Sciences in 1993 from Karolinska Institutet, Stockholm, Sweden. He also obtained a Clinical Specialty in Neurology from the Swedish Board of Health and Welfare. He published more than 100 papers in high rated scientific journals as Cell, Nature, J Exp. Med., J Immunol., etc., published more than 40 abstracts and had several International Patents. He participated in many PhD Examination Committees, acted as potential reviewer for many journals and several foundations, received several Awards and Fellowships.
Abstract:
Multiple sclerosis (MS) is a multi-factorial disease of the Central Nervous System (CNS) affecting young adults leading to significant disabilities over time. MS is now believed to be prevalent in Arabian Gulf area with high incidence due to environmental factors and unknown genetic variations. The objectives of this study was to detect up-regulated potential genes that might be involved in neuroinflammatory process in MS patients in Bahrain and to measure the protein levels of the expressed genes. A microarray was used to investigate mRNA expression from 12 MS patients and 12 control subjects in Bahrain where the mRNA came from peripheral blood leukocytes. Also, 80 MS patients and 80 control subjects were analyzed to measure serum protein levels of the expressed genes by ELISA. The data showed 15,480 genes expressed from over 47,000 transcripts and variants. Only 5 genes were significantly up-regulated in MS patients vs control subjects; namely TNF-AIP6, IL-1RA, OASL, CLC and DOCK4 (p<0.05). Conversely, KIAA0125 gene was significantly down-regulated (p<0.0003). Analysis of the effector molecules of the up-regulated genes revealed that 83 MS patients had positive serum level of OASL, 87 MS patients had positive serum levels of IL-1RA, and none of the 88 MS patients showed detectable serum levels of TNF-AIP6, CLC or DOCK4. In conclusion, OASL and IL-1RA genes were strongly expressed in MS patients and that their effector molecules may be considered as biomarkers associated with the inflammatory process of the disease and possibly treatment response.
- Biochemistry and Molecular Biology | Molecular Medicine | Innate Immunity and Inflammation | Auto Immune Diseases | Molecular Immunology | Molecular & Cellular Oncology
Location: London, UK
Chair
Giulio Tarro
Foundation de Beaumont Bonelli for Cancer Research, Italy
Co-Chair
Moiz Bakhiet
Arabian Gulf University, Bahrain
Session Introduction
Meital Charni
Weizmann Institute of Science, Israel
Title: Novel p53 target genes secreted by the liver are involved in non-cell-autonomous regulation
Biography:
Meital Charni-Natan- B.SC degree with high honors and departmental honors in life science, Ben-Gurion University of the Negev, Beer Sheva, Israel. MSc and PhD- Department of molecular cell biology, Weizmann Institute of Science, Rehovot, Israel. Thesis advisor: Prof. V. Rotter Topic: understanding the non-cell-autonomous function of the tumor suppressor p53 in the liver.
Abstract:
The tumor suppressor p53 is a transcription factor that prevents cancer development and is involved in regulation of various physiological processes. This is mediated both by induction of cell cycle arrest and apoptosis and by controlling the expression of a plethora of target genes, including secreted proteins. It has been demonstrated that p53 may exert its effect in non-cell-autonomous fashion by modulating the expression of genes that encode for secreted factors. In this study, we utilized our microarray data to identify and characterize novel p53 target genes expressed in human liver cells and associated with steroid hormones processing and transfer. We identified the steroid hormones binding factors, sex hormone binding globulin, corticosteroid-binding globulin and cytochrome P450 family 21 subfamily A polypeptide 2, as novel p53 target genes. Their expression and secretion were increased following p53 activation in various hepatic cells. We observed that p53 wild type mice exhibited higher levels of corticosteroid-binding globulin compared with their p53 null counterparts. We demonstrated that the induction of the steroid hormones binding factors can be mediated by binding to specific p53 responsive elements within their promoters. In addition, utilizing conditioned medium experiments we have shown that p53 dependent induction of sex hormone binding globulin secretion from liver cells enhances apoptosis of breast cancer cells. Moreover, depletion of sex hormone binding globulin abolished the induction of breast cancer cells death. The newly identified p53 target genes suggests a novel non-cell-autonomous tumor suppressive regulation mediated by p53 that is central for maintaining organism homeostasis.
Silvia Martina Ferrari
University of Pisa, Italy
Title: CXCL9 and CXCL10 chemokines secretion by vanadium pentoxide in primary thyroid cells
Biography:
Silvia Martina Ferrari is graduated in Biological Sciences cum laude in 2002 and specialized in Clinical Pathology in 2007 at the University of Pisa (Italy). Her principal areas of expertise are autoimmune thyroid disorders, chemokines and cytokines, type 1 diabetes, systemic autoimmune disorders, HCV-associated thyroid disorders and thyroid cancer. Her researches have been published in more than 154 articles in international journals (HI=38). She serves as an Editorial Board Member and is Referee and Reviewer of many scientific international journals.
Abstract:
Statement of the Problem: Vanadium is a grey metal, with different states of oxidation (-1, 0, +2, +3, +4, and +5), and its most common form in commercial products is vanadium pentoxide (V2O5). All vanadium compounds have been considered toxic. The exposure to a 35 mg/m3 dose of vanadium is considered life-threatening and it could provoke serious health issues, and even death, as it has been shown by The National Institute for Occupational Safety and Health. Recently it has been hypothesized a carcinogenic role of vanadium on the thyroid. However, no in vivo or in vitro studies have evaluated thyroid disruption in humans and/or animals after exposure to vanadium.
Methodology & Theoretical Orientation: Here, we evaluate the effect of V2O5 on proliferation, and chemokine secretion in normal thyrocytes.
Findings: The results of this study demonstrate that V2O5 can promote interferon-gamma dependent chemokines secretion by thyroid follicular cells, synergistically increasing the effect of Th1 important cytokines, as interferon-gamma and tumor necrosis factor-alpha, without altering their viability and proliferation. In this way, V2O5 could lead to the induction and perpetuation of an inflammatory reaction into the thyroid.
Conclusion & Significance: Further studies will be required to evaluate thyroid function, and nodules, in subjects occupationally exposed, or living in polluted areas.
Maha Bakhuraysah
Taif University, Saudi Arabia
Title: A novel immune role for NgR on b-cell populations localized in the central nervous system in a mouse model of multiple sclerosis
Biography:
Maha Bakhuraysah has her expertise in evaluation and passion in improving the health and wellbeing. Her research focuses on the role of the Nogo receptor in multiple sclerosis, she and her team are working on Experimental Autoimmune Encephalomyelitis (EAE). Previous data has mentioned that there was no new role associated with Nogo receptor, thus she focused on the immunological arm in this model and discovered the existence of B-cells expressing NgR in EAE. It has been published recently that in MS patients’ B cells are localized in the brain, which she and her team found it in mice. The studies haven't mentioned anything about the Nogo receptor, but she and her team found them too.
Abstract:
Despite clear evidence demonstrating that the deletion of Nogo-receptor 1 (NgR1) can protect against axonal degeneration and thus progression of experimental autoimmune encephalomyelitis (EAE), an immunological role for this receptor is yet to yield mechanistic evidence. However, recently NgR has been suggested as an alternate receptor for the B-cell activating factor (BAFF) in the central nervous system (CNS). Therefore, our strategic aim was to define whether NgR contributes in the modulation of the adaptive immune response during EAE by promoting maturation and differentiation of BAFF-reactive B-cells within follicles during the induction of disease. The results showed that CNS-infiltrating blood cells revealed an augmented response in the B-cells, which expressed NgR1 and NgR3, observed in ngr1+/+ mice with the onset and progression of the disease that could not be demonstrated within the spinal cords of EAE-induced ngr1-/- mice. Remarkably, a cluster of B-cells-expressing NgR was present at the meninges of lumbosacral spinal cords of the of ngr1+/+ EAE-induced mice at clinical score 1. Furthermore, there were significant increases of secreted immunoglobulins from these NgR1-expressing B-cells. Importantly, these cells could be directed into the synthesis phase of the cell cycle, after stimulating sorted cells by extracellular BAFF in vitro; however, when BAFF signaling was blocked using either rBAFF-R, or NgR1-Fc, or NgR3 peptides, the cells were observed to be into G0/G1 phase. As a consequence, when we blocked NgR1-ligand signaling using a novel hematopoietic stem cell-based delivery of a therapeutic protein, immune lineage-differentiated cells, including ZsGreen and fusion protein, were trafficking into the CNS during acute EAE. Collectively, these data indicate that the existence of an inducible expression of NgR1 and NgR3 in specific immune lineage cells upon the induction of EAE, and that the follicular-like NgR1 and NgR3-positive B-cells in the meninges may play an active role during the induction of EAE. Thus, our data reinforce the idea that blocking the interaction of BAFF and NgR1 and NgR3 may be vital for neuroprotection during inflammatory insults.
Gabriela Koifman
Weizmann Institute of Science, Israel
Title: Mutant p53 leads to enrichment of cancer stem cells that display ESC expression signature
Biography:
Gabriela Koifman did her BSc in Biotechnology and Environmental Sciences from Tel Hai academic college, MSc in Faculty of health science, Ben-Gurion University, Beer-Sheva, Israel and PhD in Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Abstract:
Mutation in the p53 gene is a frequent alteration in human cancers which mostly leads to the acquiring of new oncogenic functions that promote tumorigenesis. In this study, we observed that bone marrow derived from mutant p53 mice exhibit higher ability to form tumors compared to WT-MSCs. Cultivation of tumors obtained from mutant p53 MSCs led to the selection of aggressive tumor-derived cell lines with an enhanced tumorigenic capacity as compared with their parental MSCs. The newly established tumor-derived cell lines were able to generate tumors following injection of as few as 100 cells, as well as displayed high expression of embryonic stem cell (ESC) signature. We were able to show that the enhanced tumor initiating capacity and the expression of ESC signature exhibited by the tumor-derived cell lines is mutant p53 dependent. In order to confirm our findings in human settings, we utilized datasets from The Cancer Genome Atlas (TCGA). Expression levels of genes belonging to the ESC signature expressed by mutant p53 derived tumor cell lines were examined in human tumors harboring p53 missense mutation. In agreement with data obtained from mouse models, we identified 41 genes that were significantly and exclusively upregulated in human tumors harboring p53 missense mutation. In conclusion, our results suggest that mutant p53 oncogenic GOF in MSCs leads to the acquirement of CSC features, including enhanced expression of ESC signature. This ESC signature might assist to design a more specific cancer stem-cells targeted therapy for Li-Fraumeni patients and cancer at large.
Anastasia Dmitrieva
R-Pharm JSC, Russia
Title: Nonclinical characterization of the novel IL-1 heterodimeric fusion protein RPH-104
Biography:
Anastasia Dmitrieva has 2 years of laboratory working experience (newly derived recombinant rubella vaccine development and characterization) and 4 years experience in nonclinical studies sphere. She has organized conduction of more than 40 nonclinical studies of different medicine group: small molecules, fusion proteins, monoclonal antibodies, biosimilars, and generics. Her activities include scientific support as well as new drug and biologics license application documents review. Her area of scientific interest includes Immunology, Immune-Oncology, Biology, Virology and Pharmacology.
Abstract:
Statement of the Problem: Interleukin-1 (IL-1), a central mediator of innate immunity and inflammation, plays a pivotal role in a broad spectrum of inflammatory diseases. RPH-104 is a novel IL-1 antagonist: a heterodimer comprised of human extracellular portions of IL-1RI and IL-1 receptor accessory protein, each linked to a mutant Fc portion of human IgG1.
Aim: The aim of the studies is preclinical characterization of RPH-104.
Methodology & Theoretical Orientation: A surface plasmon resonance methods were developed to measure the binding kinetics/affinity of RPH-104 to IL-1α, IL-1β, IL-1Ra and Fc receptor binding. U937 cells which express IL-1α were selected for use in the antibody-dependent cell cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) assays. Potential tissue cross-reactivity (TCR) was assessed with histologically prepared cryo-sections from a selected panel of human and cynomolgus monkey tissues. To facilitate immunohistochemical detection RPH-104 and human IgG1 were conjugated with biotin. To assess the toxicity, toxicokinetics and immunogenicity of RPH-104, a 4 weeks subcutaneous administrations toxicity study in cynomolgus monkey was performed.
Findings: RPH-104 binds to IL-1β in preference to IL-1α or IL-Ra. RPH-104 binds to Fc (FcγRI, FcγRIIa, FcγRIIb, FcRn, FcγIIIb) receptors overall with a lower affinity than human IgG1. No evidence of RPH-104 ADCC or CDC was shown. TCR study shows similar binding of RPH-104 to cynomolgus monkeys and human tissues. There are no safety issues evident from the cynomolgus monkey GLP (Good Laboratory Practice) 4-week toxicology study. No-observed-adverse-effects-level is considered to be 100 mg/kg RPH-104.
Conclusion & Significance: Overall RPH-104 has shown potent in vitro activity and no safety concerns. This makes RPH-104 a potent candidate as an anti-inflammatory therapeutic for a range of IL-1 mediated clinical indications.
Moshe Elkabets
Ben-Gurion University of the Negev, Israel
Title: MET activation drives resistance to cetuximab in head and neck cancer
Biography:
Moshe Elkabets is an Assistant Professor in the Department of Immunology, Micriobiology and Genetics at the Ben-Gurion University of the Negev (BGU). He completed his PhD at BGU in 2011. He has two Postdocs from Harvard Medical School under the supervision of Dr. Sandra Mcallister and Jose Baselga. Then, he moved with Dr. Balsega to Memorial Sloan Kettering Cancer Center in New York. He has published 22 pre-reviewed papers, and currently his lab focuses in therapy of head and neck cancer.
Abstract:
Background: Innate and acquisition of resistance to cetuximab, an epithelial growth factor receptor (EGFR) blocker, is major problem in metastatic head and neck squamous cell carcinoma (HNSCC). Although cetuximab significantly prolongs the median overall survival in HNSCC patients, only 15% of the patients experience a partial response, which lasts only several months.
Objectives: Investigate the role of c-MET expression and localization in response to cetuximab, and elucidate the signaling pathway downstream of c-MET that is responsible for tumor cells survival and proliferation.
Methods: Genomic, transcriptomics, and proteomics profiling was done on cetuximab-sensitive (CetuxSen) and resistant tumor (CetuxRes) lesions obtained from a patient who had an exceptionally good response to cetuximab monotherapy. Immunohistochemisty, FISH, and qPCR were applied to confirm MET localization, copy number, and expression, respectively. IHC staining and analysis of MET expression were done on 20-cetuximab treated patients. Biochemical studies in vitro were conducted to uncover the molecular mechanism of resistance.
Results: MET amplification and overexpression was observed in the CetuxRes tumor compared to the CetuxSen tumor. This was accompanied by a change in localization of MET. In the CetuxSen tumor MET was expressed mainly on the cell membrane, while in the CetuxRes MET was observed in the cytoplasm, indicating for its activity. In vitro studies verified that HGF/MET pathway activation is sufficient for conferring resistance to cetuximab mainly though reactivation of the MAPK pathway.
Conclusions: We show the first clinical evidence for MET-induced resistance to cetuximab in HNSCC. Evaluation of MET expression and localization may further improve decision making when treating with cetuximab.
Biography:
Saeed El-Ashram is an Associate Professor at College of life science and Engineering, Foshan University, China. He is also the Inventor of “Compositions and methods of enhancing immune responses to Eimeria” (United States Patent 8956849). Dr. Saeed El-Ashram scientific interests include Infectious diseases, Immunology, Vaccinology, Proteomics, Immunoproteomics and Next -Generation Sequencing (MiSeq and HiSeq). His recent publications include Electrical cream separator coupled with vacuum filtration for the purification of eimerian oocysts and trichostrongylid eggs (Scientific Reports), Clustering by fast search and merge of local density peaks for gene expression microarray data (Scientific Reports), Exploring the microbial community (microflora) associated with ovine Haemonchus contortus (macroflora) field strains (Scientific Reports), Co-infection of Chlamydia psittaci with H9N2, ORT and Aspergillus fumigatus contributes to severe pneumonia and high mortality in SPF chickens(Scientific Reports), Gel Mapping to Differentiate between Sporozoites of Two Immunologically Distinct Strains of Eimeria maxima (Strains M6 and Guelph ) (PLoS One), Interferon-Gamma Release Assay,Exploring Early and Late Toxoplasma gondii Strain RH Infection by Two-Dimensional Immunoblots of Chicken Immunoglobulin G and M (PLoS One), Mycoplasma gallisepticum MGA_0676 is a membrane-associated cytotoxic nuclease with a staphylococcal nuclease region essential for nuclear (Appl Microbiol Biotechnol), and Improved Cytotoxic T Lymphocyte Responses to Vaccination with Porcine Reproductive and Respiratory Syndrome Virus in 4-1BB Transgenic Pigs (Front Immunol. 2017).
Abstract:
We have set up an ex vivo ovine abomasal model, which can mimic the multicellular process to explore the early steps in haemonchine nematode infection using RNA-seq technology. Ovine abomasal explants were collected for histological and transcriptional analysis, while supernatants were collected to quantitate lactate dehydrogenase (LDH) enzymes. A total of 233 were substantially induced genes between L4-inoculated and uninoculated-control tissues, respectively. However, a total of 14 were considerably down-regulated genes between the 51 aforementioned tissues. Fifteen pathways were annotated by Kyoto Encyclopedia of Genes and Genomes pathway analysis which accounted for the significant percentage in immediate response to larval-stage of H. contortus. Key genes upregulated in response to the addition of L4 inoculum of H. contortus were IL-6, IL-8, C1q, Atypical chemokine receptor-3, chemokine ligand-2, manganese superoxide dismutase, integrin alpha-7, -8, -9 , integrin subunit beta-1, integrin subunit beta 6, intercellular adhesion molecule-1 and actin alpha-1. This study shows for the first time that galectin-1 is up-regulated in an ex vivo abomasal segment model exposed to L4-inoculum of H. contortus following six hours of incubation. The abomasal segment model has been shown to be a suitable tool to study the haemonchine larval-stage effects on the ovine abomasal tissues prior to in vivo assessment.
Mohammad Hossein Feiz Haddad
Ahvaz Jundishapur University of Medical Sciences, Iran
Title: The study of relation among toxoplasmosis, hypothyroidism and hyperthyroidism in pregnant women, Southwest-Iran, 2017-2018
Biography:
Mohammad Hossien Feiz Hadad completed his PhD from Bradford University, England in Pharmaco-parasitology on biopharmaceutical and standard drugs for their mechanisms of action on blood and intestinal parasites. He completed his postdoctoral studies at Nottingham Trent University, England on Leishmania vaccine focus on peptide sub-unit, DNA vaccines, centrin genes and immuno-modifier molecules OX40L: TNF super family member expressing on activated dendritic cells and involved in T cell activation. He is Supervising Msc and PhD projects in Ahvaz Jundishapur University of Medical Sciences, Iran, on evaluation of anti-protozoal drug combinations, drug resistance and Protozoal ultra-structure studies. His recent research activities focused in water-borne parasites and Water treatment technologies to remove effectively parasitic elements.
Abstract:
Background: Toxoplasma gondii has a worldwide prevalence and mankind get infected by this parasite as an interface host. The parasite reaches to different parts of body through blood and lymph after the entrance. It may enter the pituitary and thyroid glands and effect the production of thyroid hormones and TSH. Thyroid disorders are relatively common among pregnant women which may cause complications such as preeclampsia, abortion, preterm delivery. Toxoplasma parasite itself could cause abortion in pregnant women and they might also lead to cerebral, ocular damages in fetus. Therefore, this study was designed to investigate the relation between toxoplasmosis and thyroid disorders in pregnant women, Southwest-Iran, 2018.
Materials & Methods: Serums of 630 pregnant women were examined for detection of Toxoplasma gondii IgG and IgM immunoglobulins and thyroid disorders through TSH test using AUTOBIO kits. The biometric and serological obtained results were analyzed by SPSS application and chi-square test.
Results: The Toxoplasma gondii IgG immunoglobulin was detected in 70.6% of the pregnant women with hyperthyroidism and there was a significant relation between above variations (p=0.001). Prevalence of Toxoplasma gondii IgG and IgM immunoglobulins were 31.9% and 1.1%, respectively. While, hypothyroidism and hyperthyroidism prevalence among pregnant women were 28.1% and 2.7% respectively and there was a statistically significant correlation between IgG immunoglobulin and education (p=0.004), contact with cats (p=0.019), and contact with soil (p=0.046) variations.
Conclusion: This study proved that there is a statistically significant correlation between hyperthyroidism and Toxoplasma gondii IgG immunoglobulin in pregnant women (p=0.001) and being infected with Toxoplasma gondii parasite can possibly be one of the reasons of hyperthyroidism among pregnant women. The hyperthyroidism complications such as spontaneous abortion, preeclampsia, heart failure, premature and low birth weight in pregnant women could be prevented by considering health measures for the avoidance of toxoplasmosis.