Associations of short-term ambient temperature exposure with lung function in middle-aged and elderly people:A longitudinal study in China

The short-term associations of ambient temperature exposure with lung function in middle-aged and elderly Chinese remain obscure.The study included 19,128 participants from the Dongfeng-Tongji cohort's first(2013)and second(2018)follow-ups.The lung function for each subject was determined between April and December 2013 and re-assessed in 2018,with three parameters(forced vital capacity[FVC],forced expiratory volume in 1 s[FEV1],and peak expiratory flow[PEF])selected.The China Meteorological Data Sharing Service Center provided temperature data during the study period.In the two follow-ups,a total of 25,511 records(average age:first,64.57;second,65.80)were evaluated,including 10,604 males(41.57%).The inversely J-shaped associations between moving average temperatures(lag01–lag07)and FVC,FEV1,and PEF were observed,and the optimum temperatures at lag04 were 16.5C,18.7C,and 16.2C,respectively.At lag04,every 1C increase in temperature was associated with 14.07 mL,9.78 mL,and 62.72 mL/s increase in FVC,FEV1,and PEF in the lowtemperature zone(<the optimum temperatures),whereas 5.72 mL,2.01 mL,and 11.64 mL/s decrease in the high-temperature zone(the optimum temperatures),respectively(all P<0.05).We observed significant effect modifications of gender,age,body mass index,body surface area,smoking status,drinking status,and physical activity on the associations(all Pmodification<0.05).Non-optimal temperatures may cause lung function decline.Several individual characters and lifestyles have effect modification on the temperature effects.

Neutralization of interleukin-11 attenuates silica particles-induced pulmonary inflammation and fibrosis in vivo

Environmental exposure to crystalline silica particles can lead to silicosis, which is one of the most serious pulmonary interstitial fibrosis around the world. Unfortunately, the exact mechanism on silicosis is unclear, and the effective treatments are lacking to date. In this study, we aim to explore the molecular mechanism by which interleukin-11(IL-11) affects silica particles-induced lung inflammation and fibrosis. We observed that IL-11 expressions in mouse lungs were significantly increased after silica exposure, and maintained at high levels across both inflammation and fibrosis phase. Immunofluorescent dual staining further revealed that the overexpression of IL-11 mainly located in mouse lung epithelial cells and fibroblasts. Using neutralizing anti-IL-11 antibody could effectively alleviate the overexpression of pro-inflammatory cytokines(i.e., interleukin-6 and tumor necrosis factor-α) and fibrotic proteins(i.e., collagen type I and matrix metalloproteinase-2) induced by silica particles. Most importantly, the expressions of IL-11 receptor subunit α(IL-11Rα), Glycoprotein130(GP130), and phosphorylated extracellular signal-regulated kinase(p-ERK) were significantly increased in response to silica, whereas blocking of IL-11 markedly reduced their levels. All findings suggested that the overexpression of IL-11 was involved in the pathological of silicosis, while neutralizing IL-11 antibody could effectively alleviate the silica-induced lung inflammation and fibrosis by inhibiting the IL-11Rα/GP130/ERK signaling pathway. IL-11 might be a promising therapeutic target for lung inflammation and fibrosis caused by silica particles exposure.