Abstract
T helper (Th) 17 cells and CD4+ CD25+ regulatory T (Treg) cells are supposed to be critically involved in regulating autoimmune and inflammatory diseases. The aim of this study was to investigate the Th17/Treg pattern in rats with gunpowder smog-induced acute lung injury. Wistar rats were equally randomized to three groups: normal control group, ALI 6 h group (smoke inhalation for 6 h) and ALI 24 h group (smoke inhalation for 24 h). We observed changes in cell counting in bronchoalveolar lavage fluid (BALF), alveolar-capillary membrane permeability and lung tissue pathology. Moreover, rats in ALI 6 h and ALI 24 h group showed increased expression of Th17 cell and related cytokines (IL-17 A, IL-6, TGF-β and IL-23). Meanwhile, Treg prevalence and related cytokines (IL-10, IL-2 and IL-35) were decreased. Consequently, the ratio of Th17/Treg was higher after smoke inhalation. Additionally, Th1 cell decreased while Th2 cell increased at 6 h and 24 h after smoke inhalation. In conclusion, Th17/Treg imbalance exists in rats with smoke inhalation-induced acute lung injury, suggesting its potential role in the pathogenesis of this disease.
Highlights
In contrast to Tregs, Th17 cell plays a potent proinflammatory role by producing the signature cytokine IL-17A
When rats were exposed to smoke for 21 min, the mortality increased with dosage of gunpowder
Despite decades of intense research, the molecular mechanisms involved in the pathogenesis of smoke inhalation-induced acute lung injury are poorly defined
Summary
In contrast to Tregs, Th17 cell plays a potent proinflammatory role by producing the signature cytokine IL-17A. 3 min 8 min 10 min studies revealed that IL-17A could act as a pro-inflammatory cytokine and may play an important role in ALI induced by lipopolysaccharide or H1N1 influenza virus[22,23]. Studies have demonstrated that both losartan and alanylglutamine may protect mice from lipopolysaccharide-induced lung injury by suppressing Th17 immune responses and modulating the Th17/Treg balance in favor of Tregs, respectively[11,25]. It has been shown that the balance between Th17 and Treg is vital in the development of autoimmune and inflammatory diseases. The role of Th17/Treg balance in smoke inhalation-induced acute lung injury is currently unknown. The aim of this study was to investigate the Th17/Treg pattern in rats with gunpowder smog-induced acute lung injury
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