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Although PM can cause adverse health effects through direct damage to host cells, our previous study showed that PM can also impact bacterial behaviour by promoting\n                    <jats:italic>in vivo<\/jats:italic>\n                    colonization. In this study we describe the genetic mechanisms involved in the bacterial response to exposure to black carbon (BC), a constituent of PM found in most sources of air pollution. We show that\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    strain USA300 LAC grown in BC prior to inoculation showed increased murine respiratory tract colonization and pulmonary invasion\n                    <jats:italic>in vivo<\/jats:italic>\n                    , as well as adhesion and invasion of human epithelial cells\n                    <jats:italic>in vitro<\/jats:italic>\n                    . Global transcriptional analysis showed that BC has a widespread effect on\n                    <jats:italic>S<\/jats:italic>\n                    .\n                    <jats:italic>aureus<\/jats:italic>\n                    transcriptional responses, altering the regulation of the major virulence gene regulators Sae and Agr and causing increased expression of genes encoding toxins, proteases and immune evasion factors. Together these data describe a previously unrecognized causative mechanism of air pollution\u2010associated infection, in that exposure to BC can increase bacterial colonization and virulence factor expression by acting directly on the bacterium rather than via the host.\n                  <\/jats:p>","DOI":"10.1111\/1462-2920.16076","type":"journal-article","created":{"date-parts":[[2022,6,1]],"date-time":"2022-06-01T06:09:41Z","timestamp":1654063781000},"page":"4449-4465","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Air pollution induces\n                    <i>Staphylococcus aureus<\/i>\n                    USA300 respiratory tract colonization mediated by specific bacterial genetic responses involving the global virulence gene regulators Agr and Sae"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4761-9949","authenticated-orcid":false,"given":"Jo","family":"Purves","sequence":"first","affiliation":[{"name":"Department of Genetics University of Leicester, University Road  Leicester LE1 7RH UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shane J. 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