Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 12, Pages 7080-7088Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1003687
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Funding
- National Institute of Allergy and Infectious Diseases (National Institutes of Health) [F31 AI061882, R01 AI081825]
- Howard Hughes Medical Institute
- Patrick and Catherine Weldon Donaghue Medical Research Foundation
- Burroughs Wellcome Fund
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The opportunistic human pathogen Pseudomonas aeruginosa causes rapidly progressive and tissue-destructive infections, such as hospital-acquired and ventilator-associated pneumonias. Innate immune responses are critical in controlling P. aeruginosa in the mammalian lung, as demonstrated by the increased susceptibility of MyD88(-/-) mice to this pathogen. Experiments conducted using bone marrow chimeric mice demonstrated that radio-resistant cells participated in initiating MyD88-dependent innate immune responses to P. aeruginosa. In this study we used a novel transgenic mouse model to demonstrate that MyD88 expression by epithelial cells is sufficient to generate a rapid and protective innate immune response following intranasal infection with P. aeruginosa. MyD88 functions as an adaptor for many TLRs. However, mice in which multiple TLR pathways (e.g., TLR2/TLR4/TLR5) are blocked are not as compromised in their response to P. aeruginosa as mice lacking MyD88. We demonstrate that IL-1R signaling is an essential element of MyD88-dependent epithelial cell responses to P. aeruginosa infection. The Journal of Immunology, 2011, 186: 7080-7088.
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