Background Th17 lymphocytes play an important role in the development of some autoimmune diseases by secreting the characteristic cytokine IL-17 to exert their strong inflammatory effects and relying on IL-23 for expansion and maintenance.
Objective This study is to investigate the role of Th17 lymphocytes and related cytokines in an asthmatic rat model exacerbated by subacute exposure to traffic related PM2.5 and its aqueous and organic extracts.
Methods Eighty SD rats weighing 180-220 g were randomly divided into eight groups, with 10 rats in each group, including saline control group, asthma control group, PM2.5 group, low-dose aqueous extract group (low AE group), high-dose aqueous extract group (high AE group), DMSO control group, low-dose organic extract group (low OE group), and high-dose organic extract group (high OE group). All the exposed groups were sensitized with ovalbumin (OVA) and challenged with aerosolized OVA to establish an asthmatic rat model. PM2.5 and its aqueous and organic extracts were intratracheally instilled into the asthmatic rats during the challenge phase to construct an asthmatic exacerbation rat model. Changes of organ coefficients and total and differential white blood cells in bronchoalveolar lavage fluid (BALF) were calculated. The expression levels of IL-17 and IL-23 in BALF were determined by ELISA. The percentages of Th17 cells in peripheral blood were measured by flow cytometry.
Results After OVA sensitization and challenge, the asthmatic rats showed obvious symptoms of wheezing, shortness of breath, forelimb contraction, and scratching face, while the rats in the saline control group had no such symptoms. The left lung coefficients of the PM2.5 group and the high AE group were significantly higher than that of the asthma control group (Ps < 0.05). PM2.5 and its aqueous or organic components induced elevated white blood cells; PM2.5 aqueous and organic extracts led to increased eosinophil percentage and decreased macrophage percentage; PM2.5 aqueous extracts resulted in elevated neutrophil percentage (Ps < 0.05). The expression levels of IL-17 in BALF of the high AE and OE groups(66.04±12.70), (57.95±7.25) pg/mL were both higher than those of the low AE and OE groups(45.32±12.66), (39.35±6.47)pg/mL (Ps < 0.05); PM2.5 induced a higher IL-23 expression level(304.78±86.08)pg/mL than any PM2.5 AE or OE groups (Ps < 0.05). The percentages of Th17 cells in the high AE and OE groups(3.76±1.44)%, (4.41±1.55)% were significantly higher than those of the low AE and OE groups(2.18±0.84)%, (2.06±0.63)%, the asthma control group(1.79±0.26)%, and the DMSO control group(1.33±0.81)% (Ps < 0.05).
Conclusion The study have demonstrated that PM2.5 and its aqueous and organic extracts aggravate asthma attacks by increasing the proportion of Th17 lymphocytes and up-regulating the expressions of IL-17 and IL-23. PM2.5 aqueous extracts have stronger toxicity to the lung than its organic extracts, and PM2.5 plays a more potent role in mediating exacerbation of asthma attacks by Th17 than its individual extracts.
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