TY  - JOUR
  - Scully, P.,MacSharry, J.,O'Mahony, D.,Lyons, A.,O'Brien, F.,Murphy, S.,Shanahan, F.,O'Mahony, L.
  - 2013
  - February
  - Cell Immunology
  - Bifidobacterium infantis suppression of Peyer's patch MIP-1 alpha and MIP-1 beta secretion during Salmonella infection correlates with increased local CD4+CD25+T cell numbers
  - Validated
  - ()
  - 281
  - 2
  - 134
  - 140
  - The outcome following infection depends on the generation of an immune response that results in control of the pathogenic microorganism, while limiting inflammatory collateral damage to the host. Bifidobacterium infantis 35624 was shown to be protective against Salmonella associated host injury via a Treg-dependent mechanism. In this study, we further examined the mechanisms by which B. infantis-induced Tregs protect against Salmonella-associated inflammation. B. infantis 35624 feeding to Salmonella-infected mice significantly reduced Peyer's patch MIP-1 alpha and MIP-1 beta secretion. Chemokine secretion was significantly inversely correlated with Peyer's patch CD4+CD25+ cell numbers. In vitro, CD25+ T cells, but not CD25- T cells, specifically inhibited TNF-alpha and IFN-gamma secretion. However, both CD25+ and CD25- T cells suppressed MIP-1 alpha and MIP-1 beta secretion to the same extent. This study suggests that although B. infantis 35624-induced Tregs correlate with inhibition of chemokine secretion within the mucosa of pathogen infected animals, indirect cellular mechanisms may play a role. (C) 2013 Elsevier Inc. All rights reserved.The outcome following infection depends on the generation of an immune response that results in control of the pathogenic microorganism, while limiting inflammatory collateral damage to the host. Bifidobacterium infantis 35624 was shown to be protective against Salmonella associated host injury via a Treg-dependent mechanism. In this study, we further examined the mechanisms by which B. infantis-induced Tregs protect against Salmonella-associated inflammation. B. infantis 35624 feeding to Salmonella-infected mice significantly reduced Peyer's patch MIP-1 alpha and MIP-1 beta secretion. Chemokine secretion was significantly inversely correlated with Peyer's patch CD4+CD25+ cell numbers. In vitro, CD25+ T cells, but not CD25- T cells, specifically inhibited TNF-alpha and IFN-gamma secretion. However, both CD25+ and CD25- T cells suppressed MIP-1 alpha and MIP-1 beta secretion to the same extent. This study suggests that although B. infantis 35624-induced Tregs correlate with inhibition of chemokine secretion within the mucosa of pathogen infected animals, indirect cellular mechanisms may play a role. (C) 2013 Elsevier Inc. All rights reserved.
  - 0008-87490008-8749
  - ://WOS:000320838800005://WOS:000320838800005
DA  - 2013/02
ER  - 

@article{V235378863,
   = {Scully,  P. and MacSharry,  J. and O'Mahony,  D. and Lyons,  A. and O'Brien,  F. and Murphy,  S. and Shanahan,  F. and O'Mahony,  L. },
   = {2013},
   = {February},
   = {Cell Immunology},
   = {Bifidobacterium infantis suppression of Peyer's patch MIP-1 alpha and MIP-1 beta secretion during Salmonella infection correlates with increased local CD4+CD25+T cell numbers},
   = {Validated},
   = {()},
   = {281},
   = {2},
  pages = {134--140},
   = {{The outcome following infection depends on the generation of an immune response that results in control of the pathogenic microorganism, while limiting inflammatory collateral damage to the host. Bifidobacterium infantis 35624 was shown to be protective against Salmonella associated host injury via a Treg-dependent mechanism. In this study, we further examined the mechanisms by which B. infantis-induced Tregs protect against Salmonella-associated inflammation. B. infantis 35624 feeding to Salmonella-infected mice significantly reduced Peyer's patch MIP-1 alpha and MIP-1 beta secretion. Chemokine secretion was significantly inversely correlated with Peyer's patch CD4+CD25+ cell numbers. In vitro, CD25+ T cells, but not CD25- T cells, specifically inhibited TNF-alpha and IFN-gamma secretion. However, both CD25+ and CD25- T cells suppressed MIP-1 alpha and MIP-1 beta secretion to the same extent. This study suggests that although B. infantis 35624-induced Tregs correlate with inhibition of chemokine secretion within the mucosa of pathogen infected animals, indirect cellular mechanisms may play a role. (C) 2013 Elsevier Inc. All rights reserved.The outcome following infection depends on the generation of an immune response that results in control of the pathogenic microorganism, while limiting inflammatory collateral damage to the host. Bifidobacterium infantis 35624 was shown to be protective against Salmonella associated host injury via a Treg-dependent mechanism. In this study, we further examined the mechanisms by which B. infantis-induced Tregs protect against Salmonella-associated inflammation. B. infantis 35624 feeding to Salmonella-infected mice significantly reduced Peyer's patch MIP-1 alpha and MIP-1 beta secretion. Chemokine secretion was significantly inversely correlated with Peyer's patch CD4+CD25+ cell numbers. In vitro, CD25+ T cells, but not CD25- T cells, specifically inhibited TNF-alpha and IFN-gamma secretion. However, both CD25+ and CD25- T cells suppressed MIP-1 alpha and MIP-1 beta secretion to the same extent. This study suggests that although B. infantis 35624-induced Tregs correlate with inhibition of chemokine secretion within the mucosa of pathogen infected animals, indirect cellular mechanisms may play a role. (C) 2013 Elsevier Inc. All rights reserved.}},
  issn = {0008-87490008-8749},
   = {://WOS:000320838800005://WOS:000320838800005},
  source = {IRIS}
}