The role of estrogen receptor β in fine particulate matter (PM2.5) organic extract-induced pulmonary inflammation in female and male mice

Fine particulate matter organic extract (Po) was reported to promote inflammation in the lung. Sex differences were reported in many inflammatory diseases. In this study, we investigated the effects of Po exposure on pulmonary inflammatory response and evaluated the role of sex in this process. While mice were exposed to 100 mu g/m(3) Po for 12 weeks by an inhalation exposure system, the lung histopathological analysis shown obvious inflammation, the cell numbers in bronchoalveolar lavage fluid (BALF) were significantly increased, and most inflammatory cytokines in BALF were upregulated. The results of factorial analysis of variance shown that there was an interaction between sex and Po exposure in the inflammatory cell numbers and the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-5 (IL-5), and growth-related oncogene/keratinocyte chemoattractant (GRO/KC). Notably, these changes and interactions were diminished while Po-exposed mice were administered with the estrogen receptor beta (ER beta) antagonist. We speculated that sex might affect the levels of inflammatory indicators in BALF of Po-exposed mice and female mice were more prone to inflammation while exposed to Po. Moreover, ER beta was involved in these processes. To our knowledge, this is the first investigation about the role of sex in Po-induced adverse effects.

Automated summary

This study investigated the effects of fine particulate matter organic extract (Po) exposure on pulmonary inflammation and assessed the role of sex in this process. The results showed that Po exposure induced lung inflammation, increased cell numbers in bronchoalveolar lavage fluid (BALF), and upregulated inflammatory cytokines in BALF. The analysis revealed an interaction between sex and Po exposure in the inflammatory cell numbers and levels of TNF-alpha, IL-5, and GRO/KC. Female mice were more susceptible to inflammation induced by Po exposure. The involvement of ER beta in these processes was also observed.