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Samithamby Jeyaseelan - One of the best experts on this subject based on the ideXlab platform.
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retraction for theivanthiran et al nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2015Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby Jeyaseelan, Richard A FlavellAbstract:Volume 80, no. 7, p. [2558–2569][1], 2012. The authors hereby retract this article. After publication, this article was found to have evidence of data duplication as follows: (i) in Fig. 5F, the GAPDH (glyceraldehyde-3-phosphate dehydrogenase) control bands for NOD2/RIP2−/− mice at 6 h and
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nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2012Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby JeyaseelanAbstract:Bacterial pneumonia remains a significant cause of mortality in the United States. The innate immune response is the first line of defense against invading bacteria. Neutrophil recruitment to the lungs is the first step in a multistep sequence leading to bacterial clearance. Ligand interaction with pattern-recognizing receptors (PRRs) leads to chemokine production, which drives neutrophils to the site of Infection. Although we demonstrated that RIP2 is important for host defense in the lungs against Escherichia Coli, the individual roles of NOD1 and NOD2 in pulmonary defense have not been addressed. Here, we explored the role of NOD2 in neutrophil-mediated host defense against an extracellular pathogen, E. Coli. We found enhanced bacterial burden and reduced neutrophil and cytokine/chemokine levels in the lungs of NOD2−/− mice following E. Coli Infection. Furthermore, we observed reduced activation of NF-κB and mitogen-activated protein kinases (MAPKs) in the lungs of NOD2−/− mice upon E. Coli challenge. Moreover, NOD2−/− neutrophils show impaired intracellular bacterial killing. Using NOD2/RIP2−/− mice, we observed bacterial burden and neutrophil accumulation in the lungs similar to those seen with NOD2−/− mice. In addition, bone marrow-derived macrophages obtained from NOD2/RIP2−/− mice demonstrate a reduction in activation of NF-κB and MAPKs similar to that seen with NOD2−/− mice in response to E. Coli. These findings unveil a previously unrecognized role of the NOD2-RIP2 axis for host defense against extracellular Gram-negative bacteria. This pathway may represent a novel target for the treatment of lung Infection/inflammation.
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receptor interacting protein 2 controls pulmonary host defense to Escherichia Coli Infection via the regulation of interleukin 17a
Infection and Immunity, 2011Co-Authors: Theivanthiran Balamayooran, Sanjay Batra, Gayathriy Balamayooran, Samithamby Jeyaseelan, Koichi S Kobayashi, Richard A FlavellAbstract:Recognition of microbial patterns by host receptors is the first step in a multistep sequence leading to neutrophil-dependent host resistance. Although the role of membrane-bound sensors in bacterial recognition has been examined in detail, the importance of cytosolic sensors in the lungs is largely unexplored. In this context, there is a major lack of understanding related to the downstream signaling mediators, such as cells and/or molecules, during acute extracellular Gram-negative bacterial pneumonia. In order to determine the role of NOD-like receptors (NLRs), we used an experimental Escherichia Coli Infection model using mice deficient in the gene coding for the NLR adaptor, receptor-interacting protein 2 (RIP2). RIP2−/− mice with E. Coli Infection displayed higher bacterial burden and reduced neutrophil recruitment and tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX expression, along with attenuated histopathological changes in the lungs. Decreased IL-17A levels were observed, along with lower numbers of IL-17A-producing T cells, in RIP2−/− mice after Infection. RIP2−/− mice also show reduced IL-6 and IL-23 levels in the lungs, along with decreased activation of STAT3 after Infection. Furthermore, activation of NF-κB and mitogen-activated protein kinases (MAPKs) and expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in the lungs of infected RIP2−/− mice were attenuated following Infection. Although neutrophil mobilization to the blood was impaired in RIP2−/− mice following Infection, the expression of CD62P, CD11a/18, CD11b, and CXCR2 on blood and lung neutrophils was not altered between infected wild-type (WT) and RIP2−/− mice. Thus, RIP2 contributes to neutrophil-dependent host defense against an extracellular Gram-negative pathogen via (i) IL-17A regulation and (ii) neutrophil mobilization to the blood.
Carmen Contreras - One of the best experts on this subject based on the ideXlab platform.
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enteropathogenic Escherichia Coli Infection in children
Current Opinion in Infectious Diseases, 2011Co-Authors: Theresa J Ochoa, Carmen ContrerasAbstract:Purpose of review Enteropathogenic Escherichia Coli (EPEC) are important diarrheal pathogens of young children. Since the diagnosis of EPEC is now based mainly on molecular criteria, there has been an important change in their prevalence. The purpose of this paper is to review the current epidemiology of EPEC Infection and the new insights into its physiopathology.
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new insights into the epidemiology of enteropathogenic Escherichia Coli Infection
Transactions of The Royal Society of Tropical Medicine and Hygiene, 2008Co-Authors: Theresa J Ochoa, Carmen Contreras, Francesca Barletta, Erik MercadoAbstract:Enteropathogenic Escherichia Coli (EPEC) are among the most important pathogens infecting children worldwide and are one of the main causes of persistent diarrhea. EPEC were originally serogroup-defined E. Coli associated with infantile diarrhea. As various mechanisms of pathogenesis have been discovered, EPEC classification has come to be based on the presence of specific genes. The eae (intimin) and bfpA (bundle-forming pilus) genes have both been used for identification of EPEC and for subdivision of this group of bacteria into typical and atypical strains. For many years typical EPEC have been considered to be the leading cause of infantile diarrhea in developing countries and were considered rare in industrialized countries. However, current data suggests that atypical EPEC are more prevalent than typical EPEC in both developing and developed countries. Moreover, the duration of diarrhea in patients infected with atypical EPEC is significantly longer than that caused by other pathogens. When comparing the isolation rates of EPEC among children with diarrhea and healthy controls without diarrhea, in general, there is a higher isolation rate in diarrhea, although not significantly higher in all studies. These inconsistencies probably are related to the study patient populations, reflecting a possible age-related susceptibility to Infection.
Sanjay Batra - One of the best experts on this subject based on the ideXlab platform.
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retraction for theivanthiran et al nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2015Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby Jeyaseelan, Richard A FlavellAbstract:Volume 80, no. 7, p. [2558–2569][1], 2012. The authors hereby retract this article. After publication, this article was found to have evidence of data duplication as follows: (i) in Fig. 5F, the GAPDH (glyceraldehyde-3-phosphate dehydrogenase) control bands for NOD2/RIP2−/− mice at 6 h and
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nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2012Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby JeyaseelanAbstract:Bacterial pneumonia remains a significant cause of mortality in the United States. The innate immune response is the first line of defense against invading bacteria. Neutrophil recruitment to the lungs is the first step in a multistep sequence leading to bacterial clearance. Ligand interaction with pattern-recognizing receptors (PRRs) leads to chemokine production, which drives neutrophils to the site of Infection. Although we demonstrated that RIP2 is important for host defense in the lungs against Escherichia Coli, the individual roles of NOD1 and NOD2 in pulmonary defense have not been addressed. Here, we explored the role of NOD2 in neutrophil-mediated host defense against an extracellular pathogen, E. Coli. We found enhanced bacterial burden and reduced neutrophil and cytokine/chemokine levels in the lungs of NOD2−/− mice following E. Coli Infection. Furthermore, we observed reduced activation of NF-κB and mitogen-activated protein kinases (MAPKs) in the lungs of NOD2−/− mice upon E. Coli challenge. Moreover, NOD2−/− neutrophils show impaired intracellular bacterial killing. Using NOD2/RIP2−/− mice, we observed bacterial burden and neutrophil accumulation in the lungs similar to those seen with NOD2−/− mice. In addition, bone marrow-derived macrophages obtained from NOD2/RIP2−/− mice demonstrate a reduction in activation of NF-κB and MAPKs similar to that seen with NOD2−/− mice in response to E. Coli. These findings unveil a previously unrecognized role of the NOD2-RIP2 axis for host defense against extracellular Gram-negative bacteria. This pathway may represent a novel target for the treatment of lung Infection/inflammation.
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receptor interacting protein 2 controls pulmonary host defense to Escherichia Coli Infection via the regulation of interleukin 17a
Infection and Immunity, 2011Co-Authors: Theivanthiran Balamayooran, Sanjay Batra, Gayathriy Balamayooran, Samithamby Jeyaseelan, Koichi S Kobayashi, Richard A FlavellAbstract:Recognition of microbial patterns by host receptors is the first step in a multistep sequence leading to neutrophil-dependent host resistance. Although the role of membrane-bound sensors in bacterial recognition has been examined in detail, the importance of cytosolic sensors in the lungs is largely unexplored. In this context, there is a major lack of understanding related to the downstream signaling mediators, such as cells and/or molecules, during acute extracellular Gram-negative bacterial pneumonia. In order to determine the role of NOD-like receptors (NLRs), we used an experimental Escherichia Coli Infection model using mice deficient in the gene coding for the NLR adaptor, receptor-interacting protein 2 (RIP2). RIP2−/− mice with E. Coli Infection displayed higher bacterial burden and reduced neutrophil recruitment and tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX expression, along with attenuated histopathological changes in the lungs. Decreased IL-17A levels were observed, along with lower numbers of IL-17A-producing T cells, in RIP2−/− mice after Infection. RIP2−/− mice also show reduced IL-6 and IL-23 levels in the lungs, along with decreased activation of STAT3 after Infection. Furthermore, activation of NF-κB and mitogen-activated protein kinases (MAPKs) and expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in the lungs of infected RIP2−/− mice were attenuated following Infection. Although neutrophil mobilization to the blood was impaired in RIP2−/− mice following Infection, the expression of CD62P, CD11a/18, CD11b, and CXCR2 on blood and lung neutrophils was not altered between infected wild-type (WT) and RIP2−/− mice. Thus, RIP2 contributes to neutrophil-dependent host defense against an extracellular Gram-negative pathogen via (i) IL-17A regulation and (ii) neutrophil mobilization to the blood.
Gayathriy Balamayooran - One of the best experts on this subject based on the ideXlab platform.
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retraction for theivanthiran et al nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2015Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby Jeyaseelan, Richard A FlavellAbstract:Volume 80, no. 7, p. [2558–2569][1], 2012. The authors hereby retract this article. After publication, this article was found to have evidence of data duplication as follows: (i) in Fig. 5F, the GAPDH (glyceraldehyde-3-phosphate dehydrogenase) control bands for NOD2/RIP2−/− mice at 6 h and
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nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2012Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby JeyaseelanAbstract:Bacterial pneumonia remains a significant cause of mortality in the United States. The innate immune response is the first line of defense against invading bacteria. Neutrophil recruitment to the lungs is the first step in a multistep sequence leading to bacterial clearance. Ligand interaction with pattern-recognizing receptors (PRRs) leads to chemokine production, which drives neutrophils to the site of Infection. Although we demonstrated that RIP2 is important for host defense in the lungs against Escherichia Coli, the individual roles of NOD1 and NOD2 in pulmonary defense have not been addressed. Here, we explored the role of NOD2 in neutrophil-mediated host defense against an extracellular pathogen, E. Coli. We found enhanced bacterial burden and reduced neutrophil and cytokine/chemokine levels in the lungs of NOD2−/− mice following E. Coli Infection. Furthermore, we observed reduced activation of NF-κB and mitogen-activated protein kinases (MAPKs) in the lungs of NOD2−/− mice upon E. Coli challenge. Moreover, NOD2−/− neutrophils show impaired intracellular bacterial killing. Using NOD2/RIP2−/− mice, we observed bacterial burden and neutrophil accumulation in the lungs similar to those seen with NOD2−/− mice. In addition, bone marrow-derived macrophages obtained from NOD2/RIP2−/− mice demonstrate a reduction in activation of NF-κB and MAPKs similar to that seen with NOD2−/− mice in response to E. Coli. These findings unveil a previously unrecognized role of the NOD2-RIP2 axis for host defense against extracellular Gram-negative bacteria. This pathway may represent a novel target for the treatment of lung Infection/inflammation.
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receptor interacting protein 2 controls pulmonary host defense to Escherichia Coli Infection via the regulation of interleukin 17a
Infection and Immunity, 2011Co-Authors: Theivanthiran Balamayooran, Sanjay Batra, Gayathriy Balamayooran, Samithamby Jeyaseelan, Koichi S Kobayashi, Richard A FlavellAbstract:Recognition of microbial patterns by host receptors is the first step in a multistep sequence leading to neutrophil-dependent host resistance. Although the role of membrane-bound sensors in bacterial recognition has been examined in detail, the importance of cytosolic sensors in the lungs is largely unexplored. In this context, there is a major lack of understanding related to the downstream signaling mediators, such as cells and/or molecules, during acute extracellular Gram-negative bacterial pneumonia. In order to determine the role of NOD-like receptors (NLRs), we used an experimental Escherichia Coli Infection model using mice deficient in the gene coding for the NLR adaptor, receptor-interacting protein 2 (RIP2). RIP2−/− mice with E. Coli Infection displayed higher bacterial burden and reduced neutrophil recruitment and tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and CXCL5/LIX expression, along with attenuated histopathological changes in the lungs. Decreased IL-17A levels were observed, along with lower numbers of IL-17A-producing T cells, in RIP2−/− mice after Infection. RIP2−/− mice also show reduced IL-6 and IL-23 levels in the lungs, along with decreased activation of STAT3 after Infection. Furthermore, activation of NF-κB and mitogen-activated protein kinases (MAPKs) and expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) in the lungs of infected RIP2−/− mice were attenuated following Infection. Although neutrophil mobilization to the blood was impaired in RIP2−/− mice following Infection, the expression of CD62P, CD11a/18, CD11b, and CXCR2 on blood and lung neutrophils was not altered between infected wild-type (WT) and RIP2−/− mice. Thus, RIP2 contributes to neutrophil-dependent host defense against an extracellular Gram-negative pathogen via (i) IL-17A regulation and (ii) neutrophil mobilization to the blood.
Balamayooran Theivanthiran - One of the best experts on this subject based on the ideXlab platform.
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retraction for theivanthiran et al nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2015Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby Jeyaseelan, Richard A FlavellAbstract:Volume 80, no. 7, p. [2558–2569][1], 2012. The authors hereby retract this article. After publication, this article was found to have evidence of data duplication as follows: (i) in Fig. 5F, the GAPDH (glyceraldehyde-3-phosphate dehydrogenase) control bands for NOD2/RIP2−/− mice at 6 h and
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nod2 signaling contributes to host defense in the lungs against Escherichia Coli Infection
Infection and Immunity, 2012Co-Authors: Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Samithamby JeyaseelanAbstract:Bacterial pneumonia remains a significant cause of mortality in the United States. The innate immune response is the first line of defense against invading bacteria. Neutrophil recruitment to the lungs is the first step in a multistep sequence leading to bacterial clearance. Ligand interaction with pattern-recognizing receptors (PRRs) leads to chemokine production, which drives neutrophils to the site of Infection. Although we demonstrated that RIP2 is important for host defense in the lungs against Escherichia Coli, the individual roles of NOD1 and NOD2 in pulmonary defense have not been addressed. Here, we explored the role of NOD2 in neutrophil-mediated host defense against an extracellular pathogen, E. Coli. We found enhanced bacterial burden and reduced neutrophil and cytokine/chemokine levels in the lungs of NOD2−/− mice following E. Coli Infection. Furthermore, we observed reduced activation of NF-κB and mitogen-activated protein kinases (MAPKs) in the lungs of NOD2−/− mice upon E. Coli challenge. Moreover, NOD2−/− neutrophils show impaired intracellular bacterial killing. Using NOD2/RIP2−/− mice, we observed bacterial burden and neutrophil accumulation in the lungs similar to those seen with NOD2−/− mice. In addition, bone marrow-derived macrophages obtained from NOD2/RIP2−/− mice demonstrate a reduction in activation of NF-κB and MAPKs similar to that seen with NOD2−/− mice in response to E. Coli. These findings unveil a previously unrecognized role of the NOD2-RIP2 axis for host defense against extracellular Gram-negative bacteria. This pathway may represent a novel target for the treatment of lung Infection/inflammation.