Pub Date : 2016-08-03DOI: 10.3844/AJISP.2016.20.28
V. Vaclav, V. Jana
Influenza remains a serious health problem and causes approximately 500,000 deaths world-wide. With current available treatments offering neither dependable protection nor a rapid cure, many have focused their attention to alternative treatments. The aim of this study was to evaluate the possible effect of a novel maitake glucan-sulforaphane combination on immune response against influenza challenge in mice. We evaluated the effects of a glucan-sulforaphane combination on basic immune reactions, virus titre and overall survival after influenza infection. Results: We found 2 weeks supplementation with this glucan-sulforaphane combination significantly improved immunosuppression caused by the viral infection. Based on these results, we conclude that the significant immunostimulation caused by this combination helps to overcome virus-dependent suppression of defense reactions and that addition of sulforaphane to glucan can improve already established biological effects of glucan.
{"title":"A Novel Glucan-Sulforaphane Combination Stimulates Immune Response to Influenza in Mouse Model","authors":"V. Vaclav, V. Jana","doi":"10.3844/AJISP.2016.20.28","DOIUrl":"https://doi.org/10.3844/AJISP.2016.20.28","url":null,"abstract":"Influenza remains a serious health problem and causes approximately 500,000 deaths world-wide. With current available treatments offering neither dependable protection nor a rapid cure, many have focused their attention to alternative treatments. The aim of this study was to evaluate the possible effect of a novel maitake glucan-sulforaphane combination on immune response against influenza challenge in mice. We evaluated the effects of a glucan-sulforaphane combination on basic immune reactions, virus titre and overall survival after influenza infection. Results: We found 2 weeks supplementation with this glucan-sulforaphane combination significantly improved immunosuppression caused by the viral infection. Based on these results, we conclude that the significant immunostimulation caused by this combination helps to overcome virus-dependent suppression of defense reactions and that addition of sulforaphane to glucan can improve already established biological effects of glucan.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"20-28"},"PeriodicalIF":0.0,"publicationDate":"2016-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.20.28","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-29DOI: 10.3844/AJISP.2016.43.48
Kralickova Milena, V. Vaclav
Numerous studies are seeking noninvasive methods to diagnose endometriosis, but a clinically applicable test is still missing. Current paper compares the current results in our search for the best diagnostic marker. We summarize that despite the extensive research on endometriosis biomarkers, timely diagnosis using specific biomarkers remains an unfilled dream.
{"title":"Endometriosis-Search for Biomarkers","authors":"Kralickova Milena, V. Vaclav","doi":"10.3844/AJISP.2016.43.48","DOIUrl":"https://doi.org/10.3844/AJISP.2016.43.48","url":null,"abstract":"Numerous studies are seeking noninvasive methods to diagnose endometriosis, but a clinically applicable test is still missing. Current paper compares the current results in our search for the best diagnostic marker. We summarize that despite the extensive research on endometriosis biomarkers, timely diagnosis using specific biomarkers remains an unfilled dream.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"43-48"},"PeriodicalIF":0.0,"publicationDate":"2016-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.43.48","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-14DOI: 10.3844/AJISP.2016.29.36
Rosymar Coutinho de Lucas, Rafael Taglialegna, C. França, F. Segato, R. Cazzaniga, C. K. Fonseca, C. Maffei
Vulvovaginal candidiasis is an opportunistic infection that affects most women in adult life, but the defense mechanism remains to be elucidated. Animals treated with estradiol were inoculated with Candida albicans having high virulence power. The experimental control consisted of animal groups treated with estradiol and animals without treatment that were inoculated with physiologic serum. The vaginal wall was collected, at different times. The material was destined to the counting of Colony Forming Units (CFU), detection of PGE2, IgE and histological staining (hematoxylin and eosin, silver and toluidine blue) for the study of the infected vaginal section. Experimental infection was predominant due to hyphae and pseudohyphae parasitism, involving the keratinized layer of the vaginal stratified squamous epithelium, without compromise submucosal or muscular layer. Furthermore, it was observed mast and polymorphonuclear cells on vaginal tissue in response to the infection. On the other hand, IgE and PGE2 participated in the response to experimental C. albicans vaginal infection. The raise in these mediators matches with the load fungal increase during the infection evolution and with the presence of mast cell. These results suggest a probable atopic component involved in the vaginal candidiasis pathogenesis.
{"title":"Immune Response, Detection of IgE and PGE2 during Vaginal Candidiasis in Mice","authors":"Rosymar Coutinho de Lucas, Rafael Taglialegna, C. França, F. Segato, R. Cazzaniga, C. K. Fonseca, C. Maffei","doi":"10.3844/AJISP.2016.29.36","DOIUrl":"https://doi.org/10.3844/AJISP.2016.29.36","url":null,"abstract":"Vulvovaginal candidiasis is an opportunistic infection that affects most women in adult life, but the defense mechanism remains to be elucidated. Animals treated with estradiol were inoculated with Candida albicans having high virulence power. The experimental control consisted of animal groups treated with estradiol and animals without treatment that were inoculated with physiologic serum. The vaginal wall was collected, at different times. The material was destined to the counting of Colony Forming Units (CFU), detection of PGE2, IgE and histological staining (hematoxylin and eosin, silver and toluidine blue) for the study of the infected vaginal section. Experimental infection was predominant due to hyphae and pseudohyphae parasitism, involving the keratinized layer of the vaginal stratified squamous epithelium, without compromise submucosal or muscular layer. Furthermore, it was observed mast and polymorphonuclear cells on vaginal tissue in response to the infection. On the other hand, IgE and PGE2 participated in the response to experimental C. albicans vaginal infection. The raise in these mediators matches with the load fungal increase during the infection evolution and with the presence of mast cell. These results suggest a probable atopic component involved in the vaginal candidiasis pathogenesis.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"29-36"},"PeriodicalIF":0.0,"publicationDate":"2016-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.29.36","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-06-28DOI: 10.3844/AJISP.2016.17.19
Mark A. Brown, J. Storsberg, C. Schmidt
Department of Clinical Sciences, Colorado State University, Fort Collins, CO 80523-1052, USA Fraunhofer Institute for Applied Polymer Research (IAP), Division of Life Science and Bioprocesses, Department of Polymers for Biomedical, Engineering, Geiselbergstraße 69, 14476 Potsdam-Golm, Germany Editorial Office, The American Journal of Immunology, S-207, 244, 5th Avenue, New York, NY, 10001 USA and S-71, 1A, 400, King William St, Adelaide, SA 5000, Australia
科罗拉多州立大学临床科学系，Fort Collins, CO 80523-1052，美国弗劳恩霍夫应用聚合物研究所(IAP)，生命科学与生物过程分部，生物医学聚合物工程系，Geiselbergstraße 69, 14476波茨坦-戈姆，德国编辑部，The American Journal of Immunology, S-207, 244, fifth Avenue, New York, NY, 10001 USA, S-71, 1A, 400, King William St, Adelaide, SA 5000, Australia
{"title":"Where the Future is Being Made Today","authors":"Mark A. Brown, J. Storsberg, C. Schmidt","doi":"10.3844/AJISP.2016.17.19","DOIUrl":"https://doi.org/10.3844/AJISP.2016.17.19","url":null,"abstract":"Department of Clinical Sciences, Colorado State University, Fort Collins, CO 80523-1052, USA Fraunhofer Institute for Applied Polymer Research (IAP), Division of Life Science and Bioprocesses, Department of Polymers for Biomedical, Engineering, Geiselbergstraße 69, 14476 Potsdam-Golm, Germany Editorial Office, The American Journal of Immunology, S-207, 244, 5th Avenue, New York, NY, 10001 USA and S-71, 1A, 400, King William St, Adelaide, SA 5000, Australia","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"17-19"},"PeriodicalIF":0.0,"publicationDate":"2016-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.17.19","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-05-21DOI: 10.3844/AJISP.2016.37.42
F. Manhal, H. A. Mohammed
The majority of patients with Lupus Nephritis (LN) usually have abnormal findings of kidney function tests. Severe glomerular damage may be observed in some patients and requires prompt therapeutic interventions. High titer levels of anti-ds-DNA antibodies may correlate to some extent with disease activity in lupus nephritis patients. The purpose of this study was to evaluate the relationship between anti-ds-DNA antibody titers and abnormal kidney function tests in patients with lupus nephritis. A total of seventy patients with lupus nephritis and fifty healthy controls were enrolled in this study. Blood samples were collected and labeled from study patients and controls for certain hematological, biochemical and immunological investigations. Anti-ds-DNA antibodies were tested by using IgG-ELISA test. It was shown that 74% of lupus nephritis patients showed positive results for anti-ds-DNA antibodies in their serum specimens (p-value <0.01). Sensitivity and specificity of the anti-ds-DNA antibody test for the diagnosis of lupus nephritis were 74 and 100%, respectively. Anaemia, hypoalbuminemia, fasting hyperglycemia and elevated blood urea nitrogen were significantly associated with lupus nephritis activity. Further studies are required to study genomic and unprecedented biomarkers associated with anti-ds-DNA antibodies in patients with lupus nephritis to develop our perception of this autoimmune disease.
{"title":"Relationship between Anti-Ds-DNA Antibodies and Abnormal Kidney Function Tests in Patients with Lupus Nephritis","authors":"F. Manhal, H. A. Mohammed","doi":"10.3844/AJISP.2016.37.42","DOIUrl":"https://doi.org/10.3844/AJISP.2016.37.42","url":null,"abstract":"The majority of patients with Lupus Nephritis (LN) usually have abnormal findings of kidney function tests. Severe glomerular damage may be observed in some patients and requires prompt therapeutic interventions. High titer levels of anti-ds-DNA antibodies may correlate to some extent with disease activity in lupus nephritis patients. The purpose of this study was to evaluate the relationship between anti-ds-DNA antibody titers and abnormal kidney function tests in patients with lupus nephritis. A total of seventy patients with lupus nephritis and fifty healthy controls were enrolled in this study. Blood samples were collected and labeled from study patients and controls for certain hematological, biochemical and immunological investigations. Anti-ds-DNA antibodies were tested by using IgG-ELISA test. It was shown that 74% of lupus nephritis patients showed positive results for anti-ds-DNA antibodies in their serum specimens (p-value <0.01). Sensitivity and specificity of the anti-ds-DNA antibody test for the diagnosis of lupus nephritis were 74 and 100%, respectively. Anaemia, hypoalbuminemia, fasting hyperglycemia and elevated blood urea nitrogen were significantly associated with lupus nephritis activity. Further studies are required to study genomic and unprecedented biomarkers associated with anti-ds-DNA antibodies in patients with lupus nephritis to develop our perception of this autoimmune disease.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"37-42"},"PeriodicalIF":0.0,"publicationDate":"2016-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.37.42","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Ortiz-Alegría, I. Cañedo-Solares, F. Vadillo-Ortega, Marisol Castillo-Castrejon, D. Correa
The neonatal IgG Fc receptor (FcRn) plays an important role in IgG homeostasis and immunity passive transfer. Fine points regarding these mechanisms, however, are still emerging. In order to obtain information about these phenomena, it is essential to have in vitro models of endothelium that express this receptor. In this study we chose two widely used models of human endothelial cells: the semi-immortalized and stable cell line HMEC-1 (CDC/USA) and the Human Umbilical Vein Endothelial Cells (HUVECs) which maintain morphological, phenotypical and functional characteristics of human micro and macro-vasculature endothelia, respectively. We found that both cells express the FcRn mRNA and protein using real-time RT-PCR, flow cytometry and confocal microscopy, respectively. We detected differences in mRNA expression levels in HUVECs among individuals. The protein was found on the cell surface but also intracellularly within vesicles. This study supports the use of two cell types as models of FcRn expression, allowing either to understand or to manipulate the mechanisms in which the receptor is involved in vivo.
{"title":"Potential of HMEC-1 Line and HUVEC Primary Culture Cells to Study the Neonatal IgG Fc Receptor in vitro","authors":"L. Ortiz-Alegría, I. Cañedo-Solares, F. Vadillo-Ortega, Marisol Castillo-Castrejon, D. Correa","doi":"10.3844/AJISP.2016.1.9","DOIUrl":"https://doi.org/10.3844/AJISP.2016.1.9","url":null,"abstract":"The neonatal IgG Fc receptor (FcRn) plays an important role in IgG homeostasis and immunity passive transfer. Fine points regarding these mechanisms, however, are still emerging. In order to obtain information about these phenomena, it is essential to have in vitro models of endothelium that express this receptor. In this study we chose two widely used models of human endothelial cells: the semi-immortalized and stable cell line HMEC-1 (CDC/USA) and the Human Umbilical Vein Endothelial Cells (HUVECs) which maintain morphological, phenotypical and functional characteristics of human micro and macro-vasculature endothelia, respectively. We found that both cells express the FcRn mRNA and protein using real-time RT-PCR, flow cytometry and confocal microscopy, respectively. We detected differences in mRNA expression levels in HUVECs among individuals. The protein was found on the cell surface but also intracellularly within vesicles. This study supports the use of two cell types as models of FcRn expression, allowing either to understand or to manipulate the mechanisms in which the receptor is involved in vivo.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2016-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.1.9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-03-17DOI: 10.3844/AJISP.2016.10.16
S. Almasi, S. Aslani, H. Poormoghim, Ali Jamshidi, Shiva Poursani, M. Mahmoudi
The Toll-Like Receptor (TLR) family is appeared to be expressed in many cell types in the immune system and plays a role in the pathogenesis of various autoimmune diseases. The expression profile and role of TLRs in Systemic Sclerosis (SSc) have been partly explained. It is aimed through this investigation to evaluate the expression pattern of TLR 4 and 5 in Peripheral Blood Mononuclear Cells (PBMCs) from SSc patients. PBMCs were isolated from whole blood of 20 SSc patients and 50 healthy individuals. Total RNA content of leukocytes was extracted. Then, cDNA was synthesized from the mRNA of the cells. Afterward, Quantitative analysis was carried out through Real-Time PCR using the TaqMan Gene Expression Assays. An over expression of TLR5 mRNA in PBMCs from SSc patients was seen in comparison to healthy individuals. Nevertheless, the gene expression of TLR4 in SSc patients remained almost equal to controls. Our findings suggest that over expression of TLR5 in SSc patients may be involved in the pathogenesis of SSc.
{"title":"Gene Expression Profiling of Toll-Like Receptor 4 and 5 in Peripheral Blood Mononuclear Cells of Patients with Systemic Sclerosis","authors":"S. Almasi, S. Aslani, H. Poormoghim, Ali Jamshidi, Shiva Poursani, M. Mahmoudi","doi":"10.3844/AJISP.2016.10.16","DOIUrl":"https://doi.org/10.3844/AJISP.2016.10.16","url":null,"abstract":"The Toll-Like Receptor (TLR) family is appeared to be expressed in many cell types in the immune system and plays a role in the pathogenesis of various autoimmune diseases. The expression profile and role of TLRs in Systemic Sclerosis (SSc) have been partly explained. It is aimed through this investigation to evaluate the expression pattern of TLR 4 and 5 in Peripheral Blood Mononuclear Cells (PBMCs) from SSc patients. PBMCs were isolated from whole blood of 20 SSc patients and 50 healthy individuals. Total RNA content of leukocytes was extracted. Then, cDNA was synthesized from the mRNA of the cells. Afterward, Quantitative analysis was carried out through Real-Time PCR using the TaqMan Gene Expression Assays. An over expression of TLR5 mRNA in PBMCs from SSc patients was seen in comparison to healthy individuals. Nevertheless, the gene expression of TLR4 in SSc patients remained almost equal to controls. Our findings suggest that over expression of TLR5 in SSc patients may be involved in the pathogenesis of SSc.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"12 1","pages":"10-16"},"PeriodicalIF":0.0,"publicationDate":"2016-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2016.10.16","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-12-31DOI: 10.3844/AJISP.2015.116.124
W. Heuser, M. Frieri, Krishan Kumar, A. Boutin
Sepsis remains a major worldwide cause of morbidity and mortality and remains amongst the leading causes of death in medical Intensive Care Units (ICUs). Increasing injury severity associated with trauma is a significant independent risk factor for sepsis and many of these patients require intensive care unit resource utilization with increased rates of mortality. There are many postulated theories regarding the mechanism surrounding the correlation between trauma and shock. One such theory evaluated the deterioration of the immune system after trauma with the activation of Damage Associated Molecular Proteins (DAMPs) and the potential role of mitochondrial release into the bloodstream following physical injury leading to the onset of the Systemic Inflammatory Response Syndrome (SIRS). Despite these proposed theories, a breach of cellular integrity seems to unravel a multitude of immunologic responses that in essence account for the deleterious symptoms associated with sepsis. The association between traumatic injury and sepsis is very complex. This review explores the multifaceted immunoinflammatory response and gives an in depth immunologic explanation of the fundamental mediators in the initiation and continuation of the inflammatory response following the loss of cellular integrity.
{"title":"Immunology of Septic Shock and Traumatic Injury: A Review","authors":"W. Heuser, M. Frieri, Krishan Kumar, A. Boutin","doi":"10.3844/AJISP.2015.116.124","DOIUrl":"https://doi.org/10.3844/AJISP.2015.116.124","url":null,"abstract":"Sepsis remains a major worldwide cause of morbidity and mortality and remains amongst the leading causes of death in medical Intensive Care Units (ICUs). Increasing injury severity associated with trauma is a significant independent risk factor for sepsis and many of these patients require intensive care unit resource utilization with increased rates of mortality. There are many postulated theories regarding the mechanism surrounding the correlation between trauma and shock. One such theory evaluated the deterioration of the immune system after trauma with the activation of Damage Associated Molecular Proteins (DAMPs) and the potential role of mitochondrial release into the bloodstream following physical injury leading to the onset of the Systemic Inflammatory Response Syndrome (SIRS). Despite these proposed theories, a breach of cellular integrity seems to unravel a multitude of immunologic responses that in essence account for the deleterious symptoms associated with sepsis. The association between traumatic injury and sepsis is very complex. This review explores the multifaceted immunoinflammatory response and gives an in depth immunologic explanation of the fundamental mediators in the initiation and continuation of the inflammatory response following the loss of cellular integrity.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"11 1","pages":"116-124"},"PeriodicalIF":0.0,"publicationDate":"2015-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2015.116.124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-12-09DOI: 10.3844/AJISP.2015.125.138
A. C. E. Leite, V. Carneiro, J. F. Nunes, André Cruz de Sousa, M. Muniz-Junqueira, M. C. M. Guimarães
Periodontal Diseases (PD) are characterized by pathological manifestation of host immune response to bacterial infection at the tooth/gingival interface. Evidences points periodontitis as a risk factor for pathological systemic conditions, such as, cardiovascular diseases and diabetes. The identification of host factors that determine their susceptibility to immune subversion can provide useful information in the pathogenesis of periodontitis. Protective acute inflammatory response fails to remove inflammatory cells, especially neutrophils, evolving to chronic, destructive and pathological lesions. T and B cells actively participate in pathogenesis of the disease. CD4+ naive T cells are activated by antigenic stimulation and differentiate into subpopulations of distinct effector cells, characterized by its specific cytokine production profiles and functions. In periodontal infection, activated Th17 and regulatory T lymphocytes (Tregs) play antagonistic roles as effector and suppressor cells, respectively. In presence of Tregs, there is a decrease in the levels of pro-inflammatory cytokines, such as, Interferon gamma (IFN-I³), Interleukin (IL) -17, Tumor Necrosis Factor (TNF) and IL-1 I², at sites of disease. Absence of Tregs may cause a variety of disorders, such as, periodontitis. The RANKL/RANK system and Osteoprotegerin (OPG) are modulators of bone resorption in periodontitis. The balance between periodontal bone resorption by osteoclasts and bone formation by osteoblasts controls bone mass. RANKL induces osteoclast differentiation and maturation and OPG inhibits RANK/RANKL interaction and prevents bone resorption. RANKL mRNA and the RANKL/OPG mRNA ratio were enhanced in chronic periodontitis. Furthermore, the role of NF-kB, FoxP3 and T-bet transcription factors were explored. Therapies for periodontitis involving cellular and molecular biology are not specific and have many side effects. Current therapies to successfully control the PD reduces clinical signs of inflammation at local sites of the disease; however, new treatments for periodontitis should address the contribution of immune cells in bone resorption, particularly in the natural course of the disease, considering its periods of remission and progression.
{"title":"Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms","authors":"A. C. E. Leite, V. Carneiro, J. F. Nunes, André Cruz de Sousa, M. Muniz-Junqueira, M. C. M. Guimarães","doi":"10.3844/AJISP.2015.125.138","DOIUrl":"https://doi.org/10.3844/AJISP.2015.125.138","url":null,"abstract":"Periodontal Diseases (PD) are characterized by pathological manifestation of host immune response to bacterial infection at the tooth/gingival interface. Evidences points periodontitis as a risk factor for pathological systemic conditions, such as, cardiovascular diseases and diabetes. The identification of host factors that determine their susceptibility to immune subversion can provide useful information in the pathogenesis of periodontitis. Protective acute inflammatory response fails to remove inflammatory cells, especially neutrophils, evolving to chronic, destructive and pathological lesions. T and B cells actively participate in pathogenesis of the disease. CD4+ naive T cells are activated by antigenic stimulation and differentiate into subpopulations of distinct effector cells, characterized by its specific cytokine production profiles and functions. In periodontal infection, activated Th17 and regulatory T lymphocytes (Tregs) play antagonistic roles as effector and suppressor cells, respectively. In presence of Tregs, there is a decrease in the levels of pro-inflammatory cytokines, such as, Interferon gamma (IFN-I³), Interleukin (IL) -17, Tumor Necrosis Factor (TNF) and IL-1 I², at sites of disease. Absence of Tregs may cause a variety of disorders, such as, periodontitis. The RANKL/RANK system and Osteoprotegerin (OPG) are modulators of bone resorption in periodontitis. The balance between periodontal bone resorption by osteoclasts and bone formation by osteoblasts controls bone mass. RANKL induces osteoclast differentiation and maturation and OPG inhibits RANK/RANKL interaction and prevents bone resorption. RANKL mRNA and the RANKL/OPG mRNA ratio were enhanced in chronic periodontitis. Furthermore, the role of NF-kB, FoxP3 and T-bet transcription factors were explored. Therapies for periodontitis involving cellular and molecular biology are not specific and have many side effects. Current therapies to successfully control the PD reduces clinical signs of inflammation at local sites of the disease; however, new treatments for periodontitis should address the contribution of immune cells in bone resorption, particularly in the natural course of the disease, considering its periods of remission and progression.","PeriodicalId":88361,"journal":{"name":"American journal of immunology","volume":"13 1","pages":"125-138"},"PeriodicalIF":0.0,"publicationDate":"2015-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3844/AJISP.2015.125.138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70190641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2015-11-12DOI: 10.3844/AJISP.2015.108.115
A. Gawish, Nahla Mohammed, Rasha A Hussein, Elsaid Galal El-Badrawy
Human Leucocyte Antigens (HLA) class II appears to play an important role in the individual’s immune response to viral infection. The present study was aimed at assessment of the relationship between HLA DRB1 alleles and the response to HCV combined therapy in Chronic Hepatitis C patients (CHC). We enrolled a total of 44 chronically infected HCV patients without Hepatitis B Virus (HBV) or Human Immunodeficiency Virus (HIV). Their mean age was 36.45±11.18 years (21-63). HLA-DRB1 typing was done by real time Polymerase Chain Reaction (PCR). ALT and Hemoglobin (Hb) levels were assessed as well as viral genotype was taken from patients' reports (HCV genotypes were 1, 2, 3 and 4 representing 13.6, 13.6, 4.5 and 68.18%, respectively). The most frequent alleles demonstrated among patients were DRB1*13 and DRB1*07 (31.8 and 36.4%, respectively). Analysis of DRB1 frequency between sustained responders and non responders revealed that DRB1*13 allele was significantly higher among sustained responders (p<0.001), while DRB1*07 allele was significantly higher among non responders (p<0.01). Female sex, HCV genotype 2 and pretreatment low serum HCV RNA level were associated with Sustained Virological Response (SVR). Also, elevated Alanine aminotransferase (ALT) level at the 1st week of therapy followed by return to baseline level at the 4th week and a decrease of the mean hemoglobin concentration at 4th week and 12th week of therapy were significantly associated with SVR. We concluded that the virological and special HLA patterns may possibly predict the response to combination therapy in CHC patients.
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