The Experts below are selected from a list of 363 Experts worldwide ranked by ideXlab platform
Tsung Teh Wu - One of the best experts on this subject based on the ideXlab platform.
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oral serum derived bovine immunoglobulin improves duodenal immune reconstitution and absorption function in patients with HIV Enteropathy
AIDS, 2013Co-Authors: David M. Asmuth, Anthony Albanese, Netanya G Sandler, Sridevi Devaraj, Thomas H Knight, Neil M Flynn, Tammy Yotter, Juan Carlos Garcia, Emily Tsuchida, Tsung Teh WuAbstract:Objectives: To examine the impact of serum-derived bovine immunoglobulin, an oral medical food known to neutralize bacterial antigen and reduce intestinal inflammation, on restoration of mucosal immunity and gastrointestinal function in individuals with HIV Enteropathy. Design: Open-label trial with intensive 8-week phase of bovine serum immunoglobulin (SBI) 2.5g twice daily with a 4-week washout period and an optional 9-month extension study. Methods: HIV Enteropathy was defined as chronic gastrointestinal symptoms including frequent loose or watery stools despite no identifiable, reversible cause. Upper endoscopy for tissue immunofluorescent antibody assay and disaccharide gut permeability/absorption studies were performed before and after 8 weeks of SBI to test mucosal immunity and gastrointestinal function. Blood was collected for markers of microbial translocation, inflammation, and collagen kinetics. A validated gastrointestinal questionnaire assessed changes in symptoms. Results: All eight participants experienced profound improvement in symptoms with reduced bowel movements/day (P ¼0.008) and improvements in stool consistency (P ¼0.008).Gut permeability was normalbefore and after the intervention, but D-xylose absorption increased in seven of eight participants. Mucosal CD4 þ lymphocyte densities increased by a median of 139.5cells/mm 2 from 213 to 322cells/mm 2 (P ¼0.016). Intestinal-fatty acid binding protein (I-FABP), a marker of enterocyte damage, initially rose in seven of eight participants after 8 weeks (P ¼0.039), and then fell below baseline in four of five who continued receiving SBI (P ¼0.12). Baseline serum I-FABP levels were negatively correlated with subsequent rise in mucosal CD4 þ lymphocyte densities (r ¼� 0.74, P ¼0.046). Conclusion: SBI significantly increases intestinal mucosal CD4 þ lymphocyte counts,
David M. Asmuth - One of the best experts on this subject based on the ideXlab platform.
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oral serum derived bovine immunoglobulin improves duodenal immune reconstitution and absorption function in patients with HIV Enteropathy
AIDS, 2013Co-Authors: David M. Asmuth, Anthony Albanese, Netanya G Sandler, Sridevi Devaraj, Thomas H Knight, Neil M Flynn, Tammy Yotter, Juan Carlos Garcia, Emily Tsuchida, Tsung Teh WuAbstract:Objectives: To examine the impact of serum-derived bovine immunoglobulin, an oral medical food known to neutralize bacterial antigen and reduce intestinal inflammation, on restoration of mucosal immunity and gastrointestinal function in individuals with HIV Enteropathy. Design: Open-label trial with intensive 8-week phase of bovine serum immunoglobulin (SBI) 2.5g twice daily with a 4-week washout period and an optional 9-month extension study. Methods: HIV Enteropathy was defined as chronic gastrointestinal symptoms including frequent loose or watery stools despite no identifiable, reversible cause. Upper endoscopy for tissue immunofluorescent antibody assay and disaccharide gut permeability/absorption studies were performed before and after 8 weeks of SBI to test mucosal immunity and gastrointestinal function. Blood was collected for markers of microbial translocation, inflammation, and collagen kinetics. A validated gastrointestinal questionnaire assessed changes in symptoms. Results: All eight participants experienced profound improvement in symptoms with reduced bowel movements/day (P ¼0.008) and improvements in stool consistency (P ¼0.008).Gut permeability was normalbefore and after the intervention, but D-xylose absorption increased in seven of eight participants. Mucosal CD4 þ lymphocyte densities increased by a median of 139.5cells/mm 2 from 213 to 322cells/mm 2 (P ¼0.016). Intestinal-fatty acid binding protein (I-FABP), a marker of enterocyte damage, initially rose in seven of eight participants after 8 weeks (P ¼0.039), and then fell below baseline in four of five who continued receiving SBI (P ¼0.12). Baseline serum I-FABP levels were negatively correlated with subsequent rise in mucosal CD4 þ lymphocyte densities (r ¼� 0.74, P ¼0.046). Conclusion: SBI significantly increases intestinal mucosal CD4 þ lymphocyte counts,
Jacques Fantini - One of the best experts on this subject based on the ideXlab platform.
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the virotoxin model of HIV 1 Enteropathy involvement of gpr15 bob and galactosylceramide in the cytopathic effects induced by HIV 1 gp120 in the ht 29 d4 intestinal cell line
Journal of Biomedical Science, 2003Co-Authors: Marc Maresca, Radhia Mahfoud, Nicolas Garmy, Donald P Kotler, Jacques Fantini, Frederic ClaytonAbstract:Background: Malabsorption and diarrhea are common, serious problems in AIDS patients, and are in part due to the incompletely understood entity HIV Enteropathy. Our prior in vitro work has shown that increased transepithelial permeability and glucose malabsorption, similar to HIV Enteropathy, are caused by HIV surface protein gp120, although the mechanism remains unclear. Results: We studied the effects of HIV surface protein gp120 on the differentiated intestinal cell line HT-29-D4, specifically the effects on microtubules, transepithelial resistance, and sodium glucose cotransport. gp120 induced extensive microtubule depolymerization, an 80% decrease in transepithelial resistance, and a 70% decrease in sodium-dependent glucose transport, changes closely paralleling those of HIV Enteropathy. The effects on transepithelial resistance were used to study potential inhibitors. Neutralizing antibodies to GPR15/Bob but not to CXCR4 (the coreceptor allowing infection with these HIV strains) inhibited these effects. Antibodies to galactosylceramide (GalCer) and a synthetic analog of GalCer also inhibited the gp120-induced changes, suggesting the involvement of GalCer-enriched lipid rafts in gp120 binding to intestinal epithelial cells. Conclusion: We conclude that direct HIV infection and gp120-induced cytopathic effects are distinct phenomena. While in vivo confirmation is needed to prove this, gp120 could be a virotoxin significantly contributing to HIV Enteropathy.
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gp120 induced bob gpr15 activation a possible cause of human immunodeficiency virus Enteropathy
American Journal of Pathology, 2001Co-Authors: Frederic Clayton, Donald P Kotler, Scott K Kuwada, Terry Morgan, Caleb Stepan, Jinqiu Kuang, James Le, Jacques FantiniAbstract:Human immunodeficiency virus (HIV)-infected patients often develop malabsorption and increased intestinal permeability with diarrhea, called HIV Enteropathy, even without enteric opportunistic infections. HIV gp120-induced calcium signaling, microtubule loss, and physiological changes resembling HIV Enteropathy were previously found in the HT-29 intestinal cell line. How gp120 caused these changes was unclear. We show that the HIV co-receptor Bob/GPR15, unlike CCR5 and CXCR4, is abundant at the basal surface of small intestinal epithelium. The gp120-induced effects on HT-29 cells were inhibited by anti-Bob neutralizing antibodies, the selective G protein inhibitor pertussis toxin, and the phospholipase inhibitor U73122, but not neutralizing antibodies to CXCR4. Gp120 strains that induced signaling in HT-29 cells also induced calcium fluxes in Bob-transfected Ghost (3) cells, whereas gp120 strains not activating HT-29 cells also did not activate Bob-transfected cells. Bob is the first HIV co-receptor shown to be abundantly expressed on the basolateral surface of intestinal epithelium. Although Bob is an inefficient infection-inducing co-receptor, it mediates viral strain-specific gp120-induced calcium signaling at low, physiologically reasonable gp120 concentrations, up to 10,000-fold lower gp120 concentrations than the principal co-receptors. Gp120-induced Bob activation is a plausible cause of HIV Enteropathy.
Deirdre L. Church - One of the best experts on this subject based on the ideXlab platform.
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Gastrointestinal Viral Load and Enteroendocrine Cell Number Are Associated with Altered Survival in HIV-1 Infected Individuals
2016Co-Authors: Guido Van Marle, Keith A Sharkey, John M Gill, Deirdre L. ChurchAbstract:Human immunodeficiency virus type 1 (HIV-1) infects and destroys cells of the immune system leading to an overt immune deficiency known as HIV acquired immunodeficiency syndrome (HIV/AIDS). The gut associated lymphoid tissue is one of the major lymphoid tissues targeted by HIV-1, and is considered a reservoir for HIV-1 replication and of major importance in CD4+ T-cell depletion. In addition to immunodeficiency, HIV-1 infection also directly causes gastrointestinal (GI) dysfunction, also known as HIV Enteropathy. This Enteropathy can manifest itself as many pathological changes in the GI tract. The objective of this study was to determine the association of gut HIV-1 infection markers with long-term survival in a cohort of men who have sex with men (MSM) enrolled pre-HAART (Highly Active Antiretroviral Therapy). We examined survival over 15-years in a cohort of 42 HIV-infected cases: In addition to CD4+ T cell counts and HIV-1 plasma viral load, multiple gut compartment (duodenum and colon) biopsies were taken by endoscopy every 6 months during the initial 3-year period. HIV-1 was cultured from tissues and phenotyped and viral loads in the gut tissues were determined. Moreover, the tissues were subjected to an extensive assessment of enteroendocrine cell distribution and pathology. The collected data was used for survival analyses, which showed that patients with higher gut tissue viral load levels had a significantly worse survival prognosis. Moreover, lower numbers of serotonin (duodenum) and somatostatin (duodenum and colon) immunoreactive cell counts in the gut tissues of patients was associated with significant lower survival prognosis. Our study, suggested tha
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gastrointestinal viral load and enteroendocrine cell number are associated with altered survival in HIV 1 infected individuals
PLOS ONE, 2013Co-Authors: Guido Van Marle, Keith A Sharkey, John M Gill, Deirdre L. ChurchAbstract:Human immunodeficiency virus type 1 (HIV-1) infects and destroys cells of the immune system leading to an overt immune deficiency known as HIV acquired immunodeficiency syndrome (HIV/AIDS). The gut associated lymphoid tissue is one of the major lymphoid tissues targeted by HIV-1, and is considered a reservoir for HIV-1 replication and of major importance in CD4+ T-cell depletion. In addition to immunodeficiency, HIV-1 infection also directly causes gastrointestinal (GI) dysfunction, also known as HIV Enteropathy. This Enteropathy can manifest itself as many pathological changes in the GI tract. The objective of this study was to determine the association of gut HIV-1 infection markers with long-term survival in a cohort of men who have sex with men (MSM) enrolled pre-HAART (Highly Active Antiretroviral Therapy). We examined survival over 15-years in a cohort of 42 HIV-infected cases: In addition to CD4+ T cell counts and HIV-1 plasma viral load, multiple gut compartment (duodenum and colon) biopsies were taken by endoscopy every 6 months during the initial 3-year period. HIV-1 was cultured from tissues and phenotyped and viral loads in the gut tissues were determined. Moreover, the tissues were subjected to an extensive assessment of enteroendocrine cell distribution and pathology. The collected data was used for survival analyses, which showed that patients with higher gut tissue viral load levels had a significantly worse survival prognosis. Moreover, lower numbers of serotonin (duodenum) and somatostatin (duodenum and colon) immunoreactive cell counts in the gut tissues of patients was associated with significant lower survival prognosis. Our study, suggested that HIV-1 pathogenesis and survival prognosis is associated with altered enteroendocrine cell numbers, which could point to a potential role for enteroendocrine function in HIV infection and pathogenesis.
Frederic Clayton - One of the best experts on this subject based on the ideXlab platform.
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the virotoxin model of HIV 1 Enteropathy involvement of gpr15 bob and galactosylceramide in the cytopathic effects induced by HIV 1 gp120 in the ht 29 d4 intestinal cell line
Journal of Biomedical Science, 2003Co-Authors: Marc Maresca, Radhia Mahfoud, Nicolas Garmy, Donald P Kotler, Jacques Fantini, Frederic ClaytonAbstract:Background: Malabsorption and diarrhea are common, serious problems in AIDS patients, and are in part due to the incompletely understood entity HIV Enteropathy. Our prior in vitro work has shown that increased transepithelial permeability and glucose malabsorption, similar to HIV Enteropathy, are caused by HIV surface protein gp120, although the mechanism remains unclear. Results: We studied the effects of HIV surface protein gp120 on the differentiated intestinal cell line HT-29-D4, specifically the effects on microtubules, transepithelial resistance, and sodium glucose cotransport. gp120 induced extensive microtubule depolymerization, an 80% decrease in transepithelial resistance, and a 70% decrease in sodium-dependent glucose transport, changes closely paralleling those of HIV Enteropathy. The effects on transepithelial resistance were used to study potential inhibitors. Neutralizing antibodies to GPR15/Bob but not to CXCR4 (the coreceptor allowing infection with these HIV strains) inhibited these effects. Antibodies to galactosylceramide (GalCer) and a synthetic analog of GalCer also inhibited the gp120-induced changes, suggesting the involvement of GalCer-enriched lipid rafts in gp120 binding to intestinal epithelial cells. Conclusion: We conclude that direct HIV infection and gp120-induced cytopathic effects are distinct phenomena. While in vivo confirmation is needed to prove this, gp120 could be a virotoxin significantly contributing to HIV Enteropathy.
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gp120 induced bob gpr15 activation a possible cause of human immunodeficiency virus Enteropathy
American Journal of Pathology, 2001Co-Authors: Frederic Clayton, Donald P Kotler, Scott K Kuwada, Terry Morgan, Caleb Stepan, Jinqiu Kuang, James Le, Jacques FantiniAbstract:Human immunodeficiency virus (HIV)-infected patients often develop malabsorption and increased intestinal permeability with diarrhea, called HIV Enteropathy, even without enteric opportunistic infections. HIV gp120-induced calcium signaling, microtubule loss, and physiological changes resembling HIV Enteropathy were previously found in the HT-29 intestinal cell line. How gp120 caused these changes was unclear. We show that the HIV co-receptor Bob/GPR15, unlike CCR5 and CXCR4, is abundant at the basal surface of small intestinal epithelium. The gp120-induced effects on HT-29 cells were inhibited by anti-Bob neutralizing antibodies, the selective G protein inhibitor pertussis toxin, and the phospholipase inhibitor U73122, but not neutralizing antibodies to CXCR4. Gp120 strains that induced signaling in HT-29 cells also induced calcium fluxes in Bob-transfected Ghost (3) cells, whereas gp120 strains not activating HT-29 cells also did not activate Bob-transfected cells. Bob is the first HIV co-receptor shown to be abundantly expressed on the basolateral surface of intestinal epithelium. Although Bob is an inefficient infection-inducing co-receptor, it mediates viral strain-specific gp120-induced calcium signaling at low, physiologically reasonable gp120 concentrations, up to 10,000-fold lower gp120 concentrations than the principal co-receptors. Gp120-induced Bob activation is a plausible cause of HIV Enteropathy.