TY  - JOUR
  - O'Mahony, D.,Murphy, S.,Boileau, T.,Park, J.,O'Brien, F.,Groeger, D.,Konieczna, P.,Ziegler, M.,Scully, P.,Shanahan, F.,Kiely, B.,O'Mahony, L.
  - 2010
  - December
  - Bmc Immunology
  - Bifidobacterium animalis AHC7 protects against pathogen-induced NF-kappa B activation in vivo
  - Validated
  - ()
  - 11
  - Background: Bifidobacteria and lactobacilli are among the early and important colonizers of the gastrointestinal tract and are generally considered to be part of a normal, healthy microbiota. It is believed that specific strains within the microbiota can influence host immune-reactivity and may play a role in protection from infection and aberrant inflammatory activity. One such strain, Bifidobacterium animalis AHC7, has been previously shown to protect against Salmonella typhimurium infection in mice and helps resolve acute idiopathic diarrhea in dogs. The aim of this study was to investigate the potential molecular and cellular mechanisms underpinning the Bifidobacterium animalis AHC7 protective effect. Results: Following 4 hours of infection with Salmonella typhimurium, NF-kappa B activation was significantly elevated in vivo in placebo and Enterococcus faecium-fed animals while Bifidobacterium animalis AHC7 consumption significantly attenuated the NF-kappa B response. In vitro anti-CD3/CD28 stimulated Peyer's patch cells secreted significantly less TNF-alpha and IFN-gamma following Bifidobacterium animalis AHC7 consumption. Stimulated cells released more IL-12p70 but this difference did not reach statistical significance. No alteration in mucosal IL-6, IL-10 or MCP-1 levels were observed. No statistically significant change in the cytokine profile of mesenteric lymph node cells was noted. In vitro, Bifidobacterium animalis AHC7 was bound by dendritic cells and induced secretion of both IL-10 and IL-12p70. In addition, co-culture of CD4+ T cells with Bifidobacterium animalis AHC7-stimulated dendritic cells resulted in a significant increase in CD25+Foxp3+ T cell numbers. Conclusion: Bifidobacterium animalis AHC7 exerts an anti-inflammatory effect via the attenuation of proinflammatory transcription factor activation in response to an infectious insult associated with modulation of proinflammatory cytokine production within the mucosa. The cellular mechanism underpinning Bifidobacterium animalis AHC7 mediated attenuation of NF-kappa B activation may include recognition of the bacterium by dendritic cells and induction of CD25+Foxp3+ T cells.Background: Bifidobacteria and lactobacilli are among the early and important colonizers of the gastrointestinal tract and are generally considered to be part of a normal, healthy microbiota. It is believed that specific strains within the microbiota can influence host immune-reactivity and may play a role in protection from infection and aberrant inflammatory activity. One such strain, Bifidobacterium animalis AHC7, has been previously shown to protect against Salmonella typhimurium infection in mice and helps resolve acute idiopathic diarrhea in dogs. The aim of this study was to investigate the potential molecular and cellular mechanisms underpinning the Bifidobacterium animalis AHC7 protective effect. Results: Following 4 hours of infection with Salmonella typhimurium, NF-kappa B activation was significantly elevated in vivo in placebo and Enterococcus faecium-fed animals while Bifidobacterium animalis AHC7 consumption significantly attenuated the NF-kappa B response. In vitro anti-CD3/CD28 stimulated Peyer's patch cells secreted significantly less TNF-alpha and IFN-gamma following Bifidobacterium animalis AHC7 consumption. Stimulated cells released more IL-12p70 but this difference did not reach statistical significance. No alteration in mucosal IL-6, IL-10 or MCP-1 levels were observed. No statistically significant change in the cytokine profile of mesenteric lymph node cells was noted. In vitro, Bifidobacterium animalis AHC7 was bound by dendritic cells and induced secretion of both IL-10 and IL-12p70. In addition, co-culture of CD4+ T cells with Bifidobacterium animalis AHC7-stimulated dendritic cells resulted in a significant increase in CD25+Foxp3+ T cell numbers. Conclusion: Bifidobacterium animalis AHC7 exerts an anti-inflammatory effect via the attenuation of proinflammatory transcription factor activation in response to an infectious insult associated with modulation of proinflammatory cytokine production within the mucosa. The cellular mechanism underpinning Bifidobacterium animalis AHC7 mediated attenuation of NF-kappa B activation may include recognition of the bacterium by dendritic cells and induction of CD25+Foxp3+ T cells.
  - 1471-21721471-2172
  - ://WOS:000285919600001://WOS:000285919600001
DA  - 2010/12
ER  - 

@article{V235379049,
   = {O'Mahony,  D. and Murphy,  S. and Boileau,  T. and Park,  J. and O'Brien,  F. and Groeger,  D. and Konieczna,  P. and Ziegler,  M. and Scully,  P. and Shanahan,  F. and Kiely,  B. and O'Mahony,  L. },
   = {2010},
   = {December},
   = {Bmc Immunology},
   = {Bifidobacterium animalis AHC7 protects against pathogen-induced NF-kappa B activation in vivo},
   = {Validated},
   = {()},
   = {11},
   = {{Background: Bifidobacteria and lactobacilli are among the early and important colonizers of the gastrointestinal tract and are generally considered to be part of a normal, healthy microbiota. It is believed that specific strains within the microbiota can influence host immune-reactivity and may play a role in protection from infection and aberrant inflammatory activity. One such strain, Bifidobacterium animalis AHC7, has been previously shown to protect against Salmonella typhimurium infection in mice and helps resolve acute idiopathic diarrhea in dogs. The aim of this study was to investigate the potential molecular and cellular mechanisms underpinning the Bifidobacterium animalis AHC7 protective effect. Results: Following 4 hours of infection with Salmonella typhimurium, NF-kappa B activation was significantly elevated in vivo in placebo and Enterococcus faecium-fed animals while Bifidobacterium animalis AHC7 consumption significantly attenuated the NF-kappa B response. In vitro anti-CD3/CD28 stimulated Peyer's patch cells secreted significantly less TNF-alpha and IFN-gamma following Bifidobacterium animalis AHC7 consumption. Stimulated cells released more IL-12p70 but this difference did not reach statistical significance. No alteration in mucosal IL-6, IL-10 or MCP-1 levels were observed. No statistically significant change in the cytokine profile of mesenteric lymph node cells was noted. In vitro, Bifidobacterium animalis AHC7 was bound by dendritic cells and induced secretion of both IL-10 and IL-12p70. In addition, co-culture of CD4+ T cells with Bifidobacterium animalis AHC7-stimulated dendritic cells resulted in a significant increase in CD25+Foxp3+ T cell numbers. Conclusion: Bifidobacterium animalis AHC7 exerts an anti-inflammatory effect via the attenuation of proinflammatory transcription factor activation in response to an infectious insult associated with modulation of proinflammatory cytokine production within the mucosa. The cellular mechanism underpinning Bifidobacterium animalis AHC7 mediated attenuation of NF-kappa B activation may include recognition of the bacterium by dendritic cells and induction of CD25+Foxp3+ T cells.Background: Bifidobacteria and lactobacilli are among the early and important colonizers of the gastrointestinal tract and are generally considered to be part of a normal, healthy microbiota. It is believed that specific strains within the microbiota can influence host immune-reactivity and may play a role in protection from infection and aberrant inflammatory activity. One such strain, Bifidobacterium animalis AHC7, has been previously shown to protect against Salmonella typhimurium infection in mice and helps resolve acute idiopathic diarrhea in dogs. The aim of this study was to investigate the potential molecular and cellular mechanisms underpinning the Bifidobacterium animalis AHC7 protective effect. Results: Following 4 hours of infection with Salmonella typhimurium, NF-kappa B activation was significantly elevated in vivo in placebo and Enterococcus faecium-fed animals while Bifidobacterium animalis AHC7 consumption significantly attenuated the NF-kappa B response. In vitro anti-CD3/CD28 stimulated Peyer's patch cells secreted significantly less TNF-alpha and IFN-gamma following Bifidobacterium animalis AHC7 consumption. Stimulated cells released more IL-12p70 but this difference did not reach statistical significance. No alteration in mucosal IL-6, IL-10 or MCP-1 levels were observed. No statistically significant change in the cytokine profile of mesenteric lymph node cells was noted. In vitro, Bifidobacterium animalis AHC7 was bound by dendritic cells and induced secretion of both IL-10 and IL-12p70. In addition, co-culture of CD4+ T cells with Bifidobacterium animalis AHC7-stimulated dendritic cells resulted in a significant increase in CD25+Foxp3+ T cell numbers. Conclusion: Bifidobacterium animalis AHC7 exerts an anti-inflammatory effect via the attenuation of proinflammatory transcription factor activation in response to an infectious insult associated with modulation of proinflammatory cytokine production within the mucosa. The cellular mechanism underpinning Bifidobacterium animalis AHC7 mediated attenuation of NF-kappa B activation may include recognition of the bacterium by dendritic cells and induction of CD25+Foxp3+ T cells.}},
  issn = {1471-21721471-2172},
   = {://WOS:000285919600001://WOS:000285919600001},
  source = {IRIS}
}