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Simpson N, Shaw R, Crepin VF, et al. The enteropathogenic Escherichia coli type III secretion system effector Map binds EBP50/NHERF1: implication for cell signalling and diarrhoea. Mol Microbiol 2006; 60:349-363. An elegant study using yeast two-hybrid to identify the EPEC T3SS effector Map as a binding partner for EBP50 (NHERF1), which also clarifies the role of Map in ultrastructural changes (brush border effacement), decreased barrier function, and diarrhea in vitro and in vivo.
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Simpson N, Shaw R, Crepin VF, et al. The enteropathogenic Escherichia coli type III secretion system effector Map binds EBP50/NHERF1: implication for cell signalling and diarrhoea. Mol Microbiol 2006; 60:349-363. An elegant study using yeast two-hybrid to identify the EPEC T3SS effector Map as a binding partner for EBP50 (NHERF1), which also clarifies the role of Map in ultrastructural changes (brush border effacement), decreased barrier function, and diarrhea in vitro and in vivo.
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Lebeis SL, Bommarius B, Parkos CA, et al. TLR signaling mediated by MyD88 is required for a protective innate immune response by neutrophils to Citrobacter rodentium. J Immunol 2007; 179:566-577. This paper shows a critical role for TLR signaling in protective host responses that lead to clearance of C. rodentium infection and resolution of colitis.
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Guttman JA, Li Y, Wickham ME, et al. Attaching and effacing pathogen-induced tight junction disruption in vivo. Cell Microbiol 2006; 8:634-645. The paper documents in-vivo redistribution of claudins 1, 3, and 5 in response to C. rodentium infection resulting in intestinal barrier dysfunction and diarrhea. These changes are dependent on EspF, but not Map.
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Guttman JA, Samji FN, Li Y, et al. Evidence that tight junctions are disrupted due to intimate bacterial contact and not inflammation during attaching and effacing pathogen infection in vivo. Infect Immun 2006; 74:6075-6084. This paper shows that mucosal inflammation is not required for C. rodentium-induced alterations in tight junctions.
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Guttman JA, Samji FN, Li Y, et al. Aquaporins contribute to diarrhoea caused by attaching and effacing bacterial pathogens. Cell Microbiol 2007; 9:131-141. By characterizing EspF and EspG-dependent redistribution of water channels AQP2 and AQP3 following C. rodentium infection, this paper makes a substantial contribution to our understanding of the mechanistic basis of infectious diarrhea.
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O'Hara JR, Skinn AC, MacNaughton WK, et al. Consequences of Citrobacter rodentium infection on enteroendocrine cells and the enteric nervous system in the mouse colon. Cell Microbiol 2006; 8:646-660. This paper shows changes in the structure and function of the enteric nervous system during C. rodentium infection, leading to alterations in signaling, gut motility, and secretion. A role for adaptive immunity in these changes was established by using severe combined immunodeficient (SCID) mice.
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•] are the first to explore the effects of acute C. rodentium infection on xenobioticmetabolism, by characterizing hepatic and renal expression of P450s, UGTs, cytokines, acute phase proteins, and nuclear receptors. Changes were compared with systemic administration of endotoxin.
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•] are the first to explore the effects of acute C. rodentium infection on xenobioticmetabolism, by characterizing hepatic and renal expression of P450s, UGTs, cytokines, acute phase proteins, and nuclear receptors. Changes were compared with systemic administration of endotoxin.
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•] are the first to explore the effects of acute C. rodentium infection on xenobiotic metabolism, by characterizing hepatic and renal expression of P450s, UGTs, cytokines, acute phase proteins, and nuclear receptors. Changes were compared with systemic administration of endotoxin.
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•] are the first to explore the effects of acute C. rodentium infection on xenobiotic metabolism, by characterizing hepatic and renal expression of P450s, UGTs, cytokines, acute phase proteins, and nuclear receptors. Changes were compared with systemic administration of endotoxin.
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Williams AE, Edwards L, Hussell T. Colonic bacterial infection abrogates eosinophilic pulmonary disease. J Infect Dis 2006; 193:223-230. This paper shows that C. rodentium infection in the colon modulates the outcome of fungal infection in the lung. Th1 immunity ameliorates C. neoformans disease, providing an exciting example of immune crosstalk between mucosal site that may have broad implications for a variety of infectious diseases.
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