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. 2015;41(10):525-34.
doi: 10.3109/01902148.2015.1096315.

Interleukin-10 modulates pulmonary neutrophilic inflammation induced by cigarette smoke exposure

Manabu Higaki  1 , Hiroo Wada  1   2 , Shinichiro Mikura  1 , Tetsuo Yasutake  1 , Masuo Nakamura  1 , Mamoru Niikura  3 , Fumie Kobayashi  3 , Hiroshi Kamma  4 , Shigeru Kamiya  3 , Kazuhiro Ito  5 , Peter J Barnes  5 , Hajime Goto  1 , Hajime Takizawa  1
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Free article

Interleukin-10 modulates pulmonary neutrophilic inflammation induced by cigarette smoke exposure

Manabu Higaki et al. Exp Lung Res. 2015.
Free article

Abstract

Aim of the study: Interleukin (IL)-10 is an anti-inflammatory cytokine, but its role in cigarette smoke (CS)-induced inflammation and chronic obstructive pulmonary disease (COPD) has not been fully elucidated. The purpose of this study was to investigate the effect of IL-10 deficiency on CS-induced pulmonary inflammation in mice in vivo and in vitro.

Materials and methods: IL-10-deficient and wild-type control mice with a C57BL6/J genetic background were exposed to CS, and inflammatory cells in bronchoalveolar lavage fluid (BALF) and mRNA of cytokines in lung were evaluated with enzyme-linked immunosorbent assay (ELISA) and reverse transcription polymerase chain reaction (RT-PCR).

Results: During 12 days of daily CS exposure to wild-type mice, neutrophil counts in BAL fluid and tumor necrosis factor (TNF)-α mRNA expression were increased, peaked at day 8, and then declined on day 12 when the level of IL-10 reached its peak. In IL-10-deficient mice, neutrophil recruitment and TNF-α mRNA levels induced by CS exposure were significantly greater than those in wild-type mice. Keratinocyte-derived chemokine (KC; murine ortholog of human CXCL8) and granulocyte macrophage colony-stimulating factor (GM-CSF) mRNA levels or matrix metalloproteinase(MMP)-9 protein levels were not correlated with neutrophil count.

Conclusions: IL-10 had a modulatory effect on CS-induced pulmonary neutrophilic inflammation and TNF-α expression in mice in vivo and therefore appears to be an important endogenous suppressor of airway neutrophilic inflammation.

Keywords: COPD; IL-10; matrix metalloproteinase-9; smoking; tumor necrosis factor-α.

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