{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T01:10:00Z","timestamp":1788484200945,"version":"build-2803163510"},"reference-count":71,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,10,5]],"date-time":"2023-10-05T00:00:00Z","timestamp":1696464000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:sec><jats:title>Purpose<\/jats:title><jats:p><jats:italic>In vivo<\/jats:italic> data indicate that mouse corneas exposed to PM<jats:sub>10<\/jats:sub> showed early perforation and thinning after infection with <jats:italic>Pseudomonas aeruginosa<\/jats:italic>. To understand the mechanisms underlying this finding, we tested the effects of PM<jats:sub>10<\/jats:sub> and the mitochondria targeted anti-oxidant SKQ1 in immortalized human corneal epithelial cells (HCET) that were challenged with <jats:italic>Pseudomonas aeruginosa<\/jats:italic> strain 19660.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Mouse corneas were infected with strain 19660 after a 2 week whole-body exposure to PM<jats:sub>10<\/jats:sub> or control air and assessed by clinical scores, slit lamp photography and western blot. HCET were exposed to 100\u03bcg\/ml PM<jats:sub>10<\/jats:sub> for 24h before challenge with strain 19660 (MOI 20). A subset of cells were pre-treated with 50nM SKQ1 for 1h before PM<jats:sub>10<\/jats:sub> exposure. Phase contrast microscopy was used to study cell morphology, cell viability was measured by an MTT assay, and ROS by DCFH-DA. Levels of pro-inflammatory markers and anti-oxidant enzymes were evaluated by RT-PCR, western blot and ELISA. Reduced glutathione (GSH) and malondialdehyde (MDA) levels were evaluated by assay kits.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>In vivo<\/jats:italic>, whole body exposure to PM<jats:sub>10<\/jats:sub> vs. control air exposed mouse corneas showed early perforation and\/or corneal thinning at 3 days post infection, accompanied by increased TNF-\u03b1 and decreased SOD2 protein levels. <jats:italic>In vitro<\/jats:italic>, PM<jats:sub>10<\/jats:sub> induced a dose dependent reduction in cell viability of HCET and significantly increased mRNA levels of pro-inflammatory molecules compared to control. Exposure to PM<jats:sub>10<\/jats:sub> before bacterial challenge further amplified the reduction in cell viability and GSH levels. Furthermore, PM<jats:sub>10<\/jats:sub> exposure also exacerbated the increase in MDA and ROS levels and phase contrast microscopy revealed more rounded cells after strain 19660 challenge. PM<jats:sub>10<\/jats:sub> exposure also further increased the mRNA and protein levels of pro-inflammatory molecules, while anti-inflammatory IL-10 was decreased. SKQ1 reversed the rounded cell morphology observed by phase contrast microscopy, increased levels of MDA, ROS and pro-inflammatory molecules, and restored IL-10.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>PM<jats:sub>10<\/jats:sub> induces decreased cell viability, oxidative stress and inflammation in HCET and has an additive effect upon bacterial challenge. SKQ1 protects against oxidative stress and inflammation induced by PM<jats:sub>10<\/jats:sub> after bacterial challenge by reversing these effects. The findings provide insight into mechanisms underlying early perforation and thinning observed in infected corneas of PM<jats:sub>10<\/jats:sub> exposed mice.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fcimb.2023.1240903","type":"journal-article","created":{"date-parts":[[2023,10,5]],"date-time":"2023-10-05T13:19:50Z","timestamp":1696511990000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":8,"title":["PM10 and Pseudomonas aeruginosa: effects on corneal epithelium"],"prefix":"10.3389","volume":"13","author":[{"given":"Mallika","family":"Somayajulu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharon A.","family":"McClellan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Farooq","family":"Muhammed","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Wright","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda D.","family":"Hazlett","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,10,5]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"210112","DOI":"10.1183\/16000617.0112-2021","article-title":"Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD","volume":"31","author":"Aghapour","year":"2022","journal-title":"Eur. 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