Female sex hormones enhance the negative effects of air pollution on lung cells

Female sex hormones enhance the negative effects of air pollution on lung cells | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Female sex hormones enhance the negative effects of air pollution on lung cells J. W Smelan, D. P. Frias, J. N.A Oliveira, B Strauss, F. Antunes, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-3837907/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract This study aims to investigate whether diesel exhaust particles (DEP) alone or associated with the hormones 17β-estradiol (E2) and progesterone (P4) can interact and alter cellular responses in the hormones and xenobiotic pathways in human bronchial cells (BEAS-2B) and human lung carcinoma (A549) in the following conditions: control (CT); 10 µg/ml DEP; 1 nM E2; 10 nM P4; 1 nM E2+ 10 µg/ml DEP and 10 nM P4+ 10 µg/ml DEP with 72 hours for hormones and 8 hours for DEP. Were studied the expression and localization of ERβ, PRβ and AhR receptors, using the immunofluorescence technique; the activation of the promoter regions ERE, PRE and XRE was using the luciferase “reporter” gene assay and were measured the following cytokines: GM-CSF, IL-6, IL-10, IL-1B, RANTES and TNF-α to determine the inflammatory response using the multiplex assay. The results showed ERβ, PRβ and AhR translocation from cytoplasm to nucleus in the presence of E2 and E2+DEP, to both cells, but the same did not occur when BEAS-2B were exposed P4 + DEP. The results related with XRE and PRE showed activation of their promoter region when cells were exposed to DEP and showed a promoter inhibition response to DEP + P4. ERE did not show any significant response. The exposition of E2 and E2+DEP increased pro-inflammatory cytokines in BEAS-2B while DEP and E2+DEP increased pro-inflammatory cytokines in A549 and the anti-inflammatory cytokine IL-10 responded to E2 in both cells. BEAS-2B present their cellular responses more intensely when exposed to E2 + DEP and an increase in the expression of ERβ and PR receptors with concomitant increase in inflammatory cytokines GM-CSF, IL-6 and TNF-α. ERE promoter region was not activated, but it does not indicate that DEP does not interfere with the oestrogen pathway, maybe for another way. As conclusion, this study corroborates the hypothesis that air pollution interferes with the pathways of female sex hormones, potentially interfering with the health of the population, especially women. Air pollution Particulat matter Lun cells Estrogens Progesterone Polycycli aromati hydrocarbons Full Text Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-3837907","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":267364686,"identity":"c297528e-cd51-43cb-bf81-0532c89ede6e","order_by":0,"name":"J. 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Were studied the expression and localization of ERβ, PRβ and AhR receptors, using the immunofluorescence technique; the activation of the promoter regions ERE, PRE and XRE was using the luciferase “reporter” gene assay and were measured the following cytokines: GM-CSF, IL-6, IL-10, IL-1B, RANTES and TNF-α to determine the inflammatory response using the multiplex assay. The results showed ERβ, PRβ and AhR translocation from cytoplasm to nucleus in the presence of E2 and E2+DEP, to both cells, but the same did not occur when BEAS-2B were exposed P4 + DEP. The results related with XRE and PRE showed activation of their promoter region when cells were exposed to DEP and showed a promoter inhibition response to DEP + P4. ERE did not show any significant response. The exposition of E2 and E2+DEP increased pro-inflammatory cytokines in BEAS-2B while DEP and E2+DEP increased pro-inflammatory cytokines in A549 and the anti-inflammatory cytokine IL-10 responded to E2 in both cells. 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