{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T13:13:16Z","timestamp":1789564396554,"version":"build-2803163510"},"reference-count":44,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2016,12,29]],"date-time":"2016-12-29T00:00:00Z","timestamp":1482969600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Int J Toxicol"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:p>\n                    Fine particulate matter (PM\n                    <jats:sub>2.5<\/jats:sub>\n                    ) and sulfur dioxide (SO\n                    <jats:sub>2<\/jats:sub>\n                    ) are 2 common air pollutants, but their toxicological effects of coexposure are still not fully clear. In this study, SO\n                    <jats:sub>2<\/jats:sub>\n                    exposure (5.6 mg\/m\n                    <jats:sup>3<\/jats:sup>\n                    ) couldn\u2019t cause obvious inflammatory responses in rat lungs. The PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure (1.5 mg\/kg body weight) increased inflammatory cell counts in bronchoalveolar lavage fluid (BALF) and some inflammation damage. Importantly, SO\n                    <jats:sub>2<\/jats:sub>\n                    and PM\n                    <jats:sub>2.5<\/jats:sub>\n                    (1.5, 6.0, and 24.0 mg\/kg) coexposure induced pathological and ultrastructural damage and raised inflammatory cells in BALF compared with the control. Also, they significantly elevated the levels of pro-inflammatory cytokines, adhesion molecule, and nitric oxide (NO) and promoted the gene expression of nuclear factor kappa B (NF-\u03baB), phosphorylated p38 (p-p38), and Toll-like receptor 4 (TLR4) in rat lungs treated with higher dose of PM\n                    <jats:sub>2.5<\/jats:sub>\n                    (6.0 and 24.0 mg\/kg) plus SO\n                    <jats:sub>2<\/jats:sub>\n                    relative to the control or SO\n                    <jats:sub>2<\/jats:sub>\n                    group, along with the decreased inhibitor of NF-\u03baB\u03b1 and increased inhibitor of NF-\u03baB kinase \u03b2 expressions. The changes in the inflammatory markers in the presence of PM\n                    <jats:sub>2.5<\/jats:sub>\n                    plus SO\n                    <jats:sub>2<\/jats:sub>\n                    were not significant compared with the PM\n                    <jats:sub>2.5<\/jats:sub>\n                    group. The results indicated that inflammatory injury and pathological and ultrastructural damage in rat lungs exposed to PM\n                    <jats:sub>2.5<\/jats:sub>\n                    plus SO\n                    <jats:sub>2<\/jats:sub>\n                    were involved in TLR4\/p38\/NF-\u03baB pathway activation accompanied by oversecretion of pro-inflammatory cytokine, adhesion molecule, and NO. It provides more useful evidence to understand the possible toxicological mechanism that PM\n                    <jats:sub>2.5<\/jats:sub>\n                    and SO\n                    <jats:sub>2<\/jats:sub>\n                    copollution exacerbate lung disease.\n                  <\/jats:p>","DOI":"10.1177\/1091581816682225","type":"journal-article","created":{"date-parts":[[2017,4,13]],"date-time":"2017-04-13T03:17:33Z","timestamp":1492053453000},"page":"165-173","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":40,"title":["Fine Particulate Matter and Sulfur Dioxide Coexposures Induce Rat Lung Pathological Injury and Inflammatory Responses Via TLR4\/p38\/NF-\u03baB Pathway"],"prefix":"10.1177","volume":"36","author":[{"given":"Ruijin","family":"Li","sequence":"first","affiliation":[{"name":"Institute of Environmental Science, Shanxi University, Taiyuan, People\u2019s Republic of 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