Absence of Poly(ADP-Ribose) Polymerase 1 Delays the Onset of Salmonella enterica Serovar Typhimurium-Induced Gut Inflammation
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Altmeyer, Matthias
Life Science Zurich Graduate School, Molecular Life Science Program, University of Zurich, 8057 Zurich, Switzerland
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Barthel, Manja
Institute of Microbiology, D-BIOL, ETH Zurich, 8093 Zurich, Switzerland
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Eberhard, Matthias
Institute of Microbiology, D-BIOL, ETH Zurich, 8093 Zurich, Switzerland
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Rehrauer, Hubert
Functional Genomics Center Zurich, 8057 Zurich, Switzerland
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Hardt, Wolf-Dietrich
Institute of Microbiology, D-BIOL, ETH Zurich, 8093 Zurich, Switzerland
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Hottiger, Michael O.
Institute of Veterinary Biochemistry and Molecular Biology, University of Zurich, 8057 Zurich, Switzerland
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Published in:
- Infection and Immunity. - American Society for Microbiology. - 2010, vol. 78, no. 8, p. 3420-3431
English
ABSTRACT
The immune system comprises an innate and an adaptive immune response to combat pathogenic agents. The human enteropathogen Salmonella enterica serovar Typhimurium invades the intestinal mucosa and triggers an early innate proinflammatory host gene response, which results in diarrheal disease. Several host factors, including transcription factors and transcription coregulators, are involved in the acute early response to Salmonella infection. We found in a mouse model of enterocolitis induced by S. Typhimurium that the absence of the nuclear protein poly(ADP-ribose) polymerase 1 (PARP1), a previously described cofactor for NF-κB-mediated proinflammatory gene expression, is associated with a delayed proinflammatory immune response after Salmonella infection. Our data reveal that PARP1 is expressed in the proliferative zone of cecum crypts, where it is required for the efficient expression of proinflammatory genes, many of which are related to interferon signaling. Consequently, animals lacking PARP1 show impaired infiltration of immune cells into the gut, with severely delayed inflammation.
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Language
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Open access status
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bronze
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Identifiers
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Persistent URL
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https://folia.unifr.ch/global/documents/110832
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