The Experts below are selected from a list of 3318 Experts worldwide ranked by ideXlab platform
Hugo C Castrofarianeto - One of the best experts on this subject based on the ideXlab platform.
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integrin αdβ2 cd11d cd18 modulates leukocyte accumulation Pathogen Clearance and pyroptosis in experimental salmonella typhimurium infection
Frontiers in Immunology, 2018Co-Authors: Danielle De Oliveira Nascimento, Adriana Vieiradeabreu, Angelica F Arcanjo, Patricia T Bozza, Guy A Zimmerman, Hugo C CastrofarianetoAbstract:β2 integrins (Coxon, Rieu et al. 1996) are critical in host defense responses to invading Pathogens and inflammation. Previously, we reported that genetic deficiency of integrin αDβ2 in mice altered outcomes in experimental systemic infections including accelerated mortality in animals infected with Salmonella enterica serovar Typhimurium (Broz, Newton et al.). Here we show that deficiency of αDβ2 results in impaired accumulation of leukocytes in response to peritoneal infection by S. Typhimurium, impaired Pathogen Clearance in vivo, defective bacterial elimination by cultured peritoneal macrophages, and enhanced pyroptosis, a unique macrophage cell death process triggered by Salmonella. Salmonella-infected animals deficient in αDβ2 had increased levels of peritoneal cytokines in addition to other markers of pyroptosis, which may contribute to inflammatory injury and increased mortality in the context of impaired bacterial killing. These observations indicate important contributions of leukocyte integrins to the host response in experimental Salmonella infection and reveal previously-unrecognized activities of αDβ2 in bacterial infection.
Adriana Vieiradeabreu - One of the best experts on this subject based on the ideXlab platform.
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integrin αdβ2 cd11d cd18 modulates leukocyte accumulation Pathogen Clearance and pyroptosis in experimental salmonella typhimurium infection
Frontiers in Immunology, 2018Co-Authors: Danielle De Oliveira Nascimento, Adriana Vieiradeabreu, Angelica F Arcanjo, Patricia T Bozza, Guy A Zimmerman, Hugo C CastrofarianetoAbstract:β2 integrins (Coxon, Rieu et al. 1996) are critical in host defense responses to invading Pathogens and inflammation. Previously, we reported that genetic deficiency of integrin αDβ2 in mice altered outcomes in experimental systemic infections including accelerated mortality in animals infected with Salmonella enterica serovar Typhimurium (Broz, Newton et al.). Here we show that deficiency of αDβ2 results in impaired accumulation of leukocytes in response to peritoneal infection by S. Typhimurium, impaired Pathogen Clearance in vivo, defective bacterial elimination by cultured peritoneal macrophages, and enhanced pyroptosis, a unique macrophage cell death process triggered by Salmonella. Salmonella-infected animals deficient in αDβ2 had increased levels of peritoneal cytokines in addition to other markers of pyroptosis, which may contribute to inflammatory injury and increased mortality in the context of impaired bacterial killing. These observations indicate important contributions of leukocyte integrins to the host response in experimental Salmonella infection and reveal previously-unrecognized activities of αDβ2 in bacterial infection.
Sharon A Tooze - One of the best experts on this subject based on the ideXlab platform.
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wipi2 links lc3 conjugation with pi3p autophagosome formation and Pathogen Clearance by recruiting atg12 5 16l1
Molecular Cell, 2014Co-Authors: Hannah C Dooley, Minoo Razi, Hannah E J Polson, Stephen E Girardin, M Wilson, Sharon A ToozeAbstract:Mammalian cell homeostasis during starvation depends on initiation of autophagy by endoplasmic reticulum-localized phosphatidylinositol 3-phosphate (PtdIns(3)P) synthesis. Formation of double-membrane autophagosomes that engulf cytosolic components requires the LC3-conjugating Atg12–5-16L1 complex. The molecular mechanisms of Atg12–5-16L1 recruitment and significance of PtdIns(3)P synthesis at autophagosome formation sites are unknown. By identifying interacting partners of WIPIs, WD-repeat PtdIns(3)P effector proteins, we found that Atg16L1 directly binds WIPI2b. Mutation experiments and ectopic localization of WIPI2b to plasma membrane show that WIPI2b is a PtdIns(3)P effector upstream of Atg16L1 and is required for LC3 conjugation and starvation-induced autophagy through recruitment of the Atg12–5-16L1 complex. Atg16L1 mutants, which do not bind WIPI2b but bind FIP200, cannot rescue starvation-induced autophagy in Atg16L1-deficient MEFs. WIPI2b is also required for autophagic Clearance of Pathogenic bacteria. WIPI2b binds the membrane surrounding Salmonella and recruits the Atg12–5-16L1 complex, initiating LC3 conjugation, autophagosomal membrane formation, and engulfment of Salmonella.
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WIPI2 Links LC3 Conjugation with PI3P, Autophagosome Formation, and Pathogen Clearance by Recruiting Atg12–5-16L1
Molecular Cell, 2014Co-Authors: Hannah C Dooley, Minoo Razi, Hannah E J Polson, Stephen E Girardin, M Wilson, Sharon A ToozeAbstract:Mammalian cell homeostasis during starvation depends on initiation of autophagy by endoplasmic reticulum-localized phosphatidylinositol 3-phosphate (PtdIns(3)P) synthesis. Formation of double-membrane autophagosomes that engulf cytosolic components requires the LC3-conjugating Atg12–5-16L1 complex. The molecular mechanisms of Atg12–5-16L1 recruitment and significance of PtdIns(3)P synthesis at autophagosome formation sites are unknown. By identifying interacting partners of WIPIs, WD-repeat PtdIns(3)P effector proteins, we found that Atg16L1 directly binds WIPI2b. Mutation experiments and ectopic localization of WIPI2b to plasma membrane show that WIPI2b is a PtdIns(3)P effector upstream of Atg16L1 and is required for LC3 conjugation and starvation-induced autophagy through recruitment of the Atg12–5-16L1 complex. Atg16L1 mutants, which do not bind WIPI2b but bind FIP200, cannot rescue starvation-induced autophagy in Atg16L1-deficient MEFs. WIPI2b is also required for autophagic Clearance of Pathogenic bacteria. WIPI2b binds the membrane surrounding Salmonella and recruits the Atg12–5-16L1 complex, initiating LC3 conjugation, autophagosomal membrane formation, and engulfment of Salmonella.
Danielle De Oliveira Nascimento - One of the best experts on this subject based on the ideXlab platform.
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integrin αdβ2 cd11d cd18 modulates leukocyte accumulation Pathogen Clearance and pyroptosis in experimental salmonella typhimurium infection
Frontiers in Immunology, 2018Co-Authors: Danielle De Oliveira Nascimento, Adriana Vieiradeabreu, Angelica F Arcanjo, Patricia T Bozza, Guy A Zimmerman, Hugo C CastrofarianetoAbstract:β2 integrins (Coxon, Rieu et al. 1996) are critical in host defense responses to invading Pathogens and inflammation. Previously, we reported that genetic deficiency of integrin αDβ2 in mice altered outcomes in experimental systemic infections including accelerated mortality in animals infected with Salmonella enterica serovar Typhimurium (Broz, Newton et al.). Here we show that deficiency of αDβ2 results in impaired accumulation of leukocytes in response to peritoneal infection by S. Typhimurium, impaired Pathogen Clearance in vivo, defective bacterial elimination by cultured peritoneal macrophages, and enhanced pyroptosis, a unique macrophage cell death process triggered by Salmonella. Salmonella-infected animals deficient in αDβ2 had increased levels of peritoneal cytokines in addition to other markers of pyroptosis, which may contribute to inflammatory injury and increased mortality in the context of impaired bacterial killing. These observations indicate important contributions of leukocyte integrins to the host response in experimental Salmonella infection and reveal previously-unrecognized activities of αDβ2 in bacterial infection.
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Integrin αDβ2 (CD11d/CD18) Modulates Leukocyte Accumulation, Pathogen Clearance, and Pyroptosis in Experimental Salmonella Typhimurium Infection.
Frontiers in Immunology, 2018Co-Authors: Danielle De Oliveira Nascimento, Angelica F Arcanjo, Patricia T Bozza, Guy A Zimmerman, Adriana Vieira-de-abreu, Hugo C. Castro-faria-netoAbstract:β2 integrins (Coxon, Rieu et al. 1996) are critical in host defense responses to invading Pathogens and inflammation. Previously, we reported that genetic deficiency of integrin αDβ2 in mice altered outcomes in experimental systemic infections including accelerated mortality in animals infected with Salmonella enterica serovar Typhimurium (Broz, Newton et al.). Here we show that deficiency of αDβ2 results in impaired accumulation of leukocytes in response to peritoneal infection by S. Typhimurium, impaired Pathogen Clearance in vivo, defective bacterial elimination by cultured peritoneal macrophages, and enhanced pyroptosis, a unique macrophage cell death process triggered by Salmonella. Salmonella-infected animals deficient in αDβ2 had increased levels of peritoneal cytokines in addition to other markers of pyroptosis, which may contribute to inflammatory injury and increased mortality in the context of impaired bacterial killing. These observations indicate important contributions of leukocyte integrins to the host response in experimental Salmonella infection and reveal previously-unrecognized activities of αDβ2 in bacterial infection.
T Hussell - One of the best experts on this subject based on the ideXlab platform.
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tgf β prevents eosinophilic lung disease but impairs Pathogen Clearance
Microbes and Infection, 2005Co-Authors: Andy Williams, Ian R Humphreys, Megan Cornere, Lorna Edwards, T HussellAbstract:Respiratory infections are the third leading cause of death worldwide. Complications arise directly as a consequence of Pathogen replication or indirectly due to aberrant or excessive immune responses. In the following report, we evaluate the efficacy, in a murine model, of nasally delivered DNA encoding TGF-beta1 to suppress immunopathology in response to a variety of infectious agents. A single nasal administration suppressed lymphocyte responses to Cryptococcus neoformans, influenza virus and respiratory syncytial virus. The suppression did not depend on the phenotype of the responding T cell, since both Th1 and Th2 responses were affected. During Th2-inducing infection, pulmonary eosinophilic responses were significantly suppressed. In all cases, however, suppressed immunity correlated with increased susceptibility to infection. We conclude that nasal TGF-beta treatment could be used to prevent pulmonary, Pathogen-driven eosinophilic disease, although anti-Pathogen strategies will need to be administered concordantly.
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TGF-beta prevents eosinophilic lung disease but impairs Pathogen Clearance.
Microbes Infect, 2005Co-Authors: T HussellAbstract:Respiratory infections are the third leading cause of death worldwide. Complications arise directly as a consequence of Pathogen replication or indirectly due to aberrant or excessive immune responses. In the following report, we evaluate the efficacy, in a murine model, of nasally delivered DNA encoding TGF-beta1 to suppress immunopathology in response to a variety of infectious agents. A single nasal administration suppressed lymphocyte responses to Cryptococcus neoformans, influenza virus and respiratory syncytial virus. The suppression did not depend on the phenotype of the responding T cell, since both Th1 and Th2 responses were affected. During Th2-inducing infection, pulmonary eosinophilic responses were significantly suppressed. In all cases, however, suppressed immunity correlated with increased susceptibility to infection. We conclude that nasal TGF-beta treatment could be used to prevent pulmonary, Pathogen-driven eosinophilic disease, although anti-Pathogen strategies will need to be administered concordantly.