Premium
T c17 cells are associated with cigarette smoke‐induced lung inflammation and emphysema
Author(s) -
Zhou Hongbin,
Hua Wen,
Jin Yan,
Zhang Chao,
Che Luanqing,
Xia Lixia,
Zhou Jiesen,
Chen Zhihua,
Li Wen,
Shen Huahao
Publication year - 2015
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/resp.12486
Subject(s) - medicine , immunology , inflammation , lung , flow cytometry , t cell , cytotoxic t cell , immune system , pathology , biology , biochemistry , in vitro
Background and objective Some types of T lymphocytes, especially cytotoxic T ‐cells ( T c1) and T ‐helper ( T h17) cells, play a pivotal role in cigarette smoke‐induced lung diseases. However, whether T c17 cells are involved remains largely unknown. We investigated T c17 involvement using a cigarette smoke‐exposure model. Methods Groups of mice were exposed to cigarette smoke or filtered air. At weeks 2, 8, 12 and 24, mice were sacrificed to observe histological changes by HE stain and/or immunohistochemical staining. The frequency of T cell subsets in the lung and spleen were detected by flow cytometry. In addition, the expression levels of T cell‐related factors were measured by real‐time polymerase chain reaction or enzyme‐linked immunosorbent assay. Results Cigarette smoke caused substantial inflammatory cell infiltration and led to emphysema. Cigarette smoke exposure promoted the expression of interferon‐gamma ( IFN )‐γ and interleukin ( IL )‐17 A at the messenger ribonucleic acid and protein levels. In addition to T c1 and T h17 cells, pulmonary and splenic T c17 cells increased, which was accompanied by the upregulation of cytokines IL ‐6, transforming growth factor beta ( TGF )‐β) and transcriptional factors S tat3 and RAR‐related orphan receptor gamma. Compared with untreated mice, γ H 2 AX ‐positive cells were more frequently observed in mice exposed to cigarette smoke. Conclusions Long‐term cigarette smoke exposure induced T c17 cell expansion both locally and distally, which was associated with emphysema and deoxyribonucleic acid damage. As an important source of IL ‐17 A , this T cell subset may be a potential target for chronic obstructive pulmonary disease therapy.