کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3064502 | 1580436 | 2011 | 9 صفحه PDF | دانلود رایگان |
Utilizing a murine model of S. pneumoniae infection and restraint stress, we determined how corticotropin releasing hormone (CRH-R) receptors impacts disease. CRH-R1 (antalarmin) and CRH-R2 (astressin2B) antagonists were administered intraperitoneally prior to restraint stress followed by pulmonary S. pneumoniae infection. CRH-R1 inhibition is not protective against pneumococcal disease induced by stress. Conversely, CRH-R2 inhibition attenuates stress-induced bacterial growth and significantly prevented severe sepsis. Neutrophillic responses were associated with CRH receptor-specific disease outcome providing a potential cellular target for stress-induced susceptibility to the development of severe pneumococcal disease. CRH receptor-mediated effects on immune responses could prove valuable for novel therapeutics.
Journal: Journal of Neuroimmunology - Volume 237, Issues 1–2, 15 August 2011, Pages 57–65