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KMID : 0620920130450010006
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Experimental & Molecular Medicine
2013 Volume.45 No. 1 p.6 ~ p.0
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Acetyl salicylic acid inhibits Th17 airway inflammation via blockade of IL-6 and IL-17 positive feedback
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Moon Hyung-Geun
Kang Chil-Sung
Choi Jun-Pyo
Choi Dong-Sic
Choi Hyun-Il
Choi Yong-Wook
Jeon Seong-Gyu
Yoo Joo-Yeon
Jang Myoung-Ho
Gho Yong-Song
Kim Yoon-Keun
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Abstract
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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-17 positive feedback.
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KEYWORD
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Acetyl salicylic acid, IL-6, IL-17A, STAT3, Th17
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