期刊
CELLULAR MICROBIOLOGY
卷 7, 期 4, 页码 489-497出版社
WILEY
DOI: 10.1111/j.1462-5822.2004.00473.x
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资金
- NHLBI NIH HHS [R01 HL067871, R01 HL067871-03, R01 HL67871] Funding Source: Medline
- NIAID NIH HHS [R01 AI049346] Funding Source: Medline
- NIDCR NIH HHS [R01 DE14897, R01 DE014897] Funding Source: Medline
Expression of innate immune genes such as beta-defensins is induced in airway epithelium by bacterial components via activation of NF-kappa B. We show here that live Gram-negative bacteria can similarly stimulate this pathway, resulting in upregulation of the beta-defensin tracheal antimicrobial peptide (TAP) in primary cultures of bovine tracheal epithelial cells (TECs), by a Toll-like receptor 4 (TLR4)-mediated pathway. The Gram-negative airway pathogen Bordetella bronchiseptica possesses a type III secretion system previously suggested to inhibit the nuclear translocation of NF-kappa B in a cell line by immunohistochemistry. We therefore hypothesized that this pathogen might interfere in the innate immune response of the epithelium. Exposure of TECs to wild-type B. bronchiseptica suppressed the activation of NF-kappa B and the subsequent induction of TAP mRNA levels, whereas a type III secretion-defective strain did not. These results suggest a mechanism for bacterial evasion of the innate immune response in the airway, which could allow for the observed persistent colonization of this pathogen.
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