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- 자료유형
- 학술저널
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- 발행연도
- 2013.1
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T-helper (Th)17 cell responses are important for the development of neutrophilic inflammatory disease. Recently, we found that acetyl salicylic acid (ASA) inhibited Th17 airway inflammation in an asthma mouse model induced by sensitization with lipopolysaccharide (LPS)-containing allergens. To investigate the mechanism(s) of the inhibitory effect of ASA on the development of Th17 airway inflammation, a neutrophilic asthma mouse model was generated by intranasal sensitization with LPS plus ovalbumin (OVA) and then challenged with OVA alone. Immunologic parameters and airway inflammation were evaluated 6 and 48 h after the last OVA challenge. ASA inhibited the production of interleukin (IL)-17 from lung T cells as well as in vitro Th17 polarization induced by IL-6. Additionally, ASA, but not salicylic acid, suppressed Th17 airway inflammation,which was associated with decreased expression of acetyl-STAT3 (downstream signaling of IL-6) in the lung. Moreover, the production of IL-6 from inflammatory cells, induced by IL-17, was abolished by treatment with ASA, whereas that induced by LPS was not. Altogether, ASA, likely via its acetyl moiety, inhibits Th17 airway inflammation by blockade of IL-6 and IL-17positive feedback.
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참고문헌 (25)
참고문헌 신청
[학술지(정기간행물)]
Bateman ED / 2008 / Global strategy for asthma management and prevention: GINA executive summary / Eur Respir J 31 : 143 ~ 178
Busse WW / 2001 / Asthma / N Engl J Med 344 : 350 ~ 362
Cla`ria J / 1995 / Aspirin triggers previously undescribed bioactive eicosanoids by human endothelial cell-leukocyte interactions / Proc Natl Acad Sci USA 92 : 9475 ~ 9479
Cronstein BN / 1999 / Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhib
Bateman ED / 2008 / Global strategy for asthma management and prevention: GINA executive summary / Eur Respir J 31 : 143 ~ 178
Busse WW / 2001 / Asthma / N Engl J Med 344 : 350 ~ 362
Cla`ria J / 1995 / Aspirin triggers previously undescribed bioactive eicosanoids by human endothelial cell-leukocyte interactions / Proc Natl Acad Sci USA 92 : 9475 ~ 9479
Cronstein BN / 1999 / Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhib
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