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In this commentary, we describe how <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s interact with the immune and non\u2010immune cells, both within and below the cervicovaginal mucosal barrier, to cause inflammation, which in turn has been associated with increased <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> acquisition risk.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s have a major impact on the female genital mucosa, which is an important biological and physical barrier that forms the first line of defence against invading microorganisms such as <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>. Pattern recognition of <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content> pathogens, by receptors expressed either on the cell surface or inside the cell, typically triggers inflammation at the mucosal barrier. The types of mucosal responses vary by <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>, and can be asymptomatic or culminate in the formation of discharge, ulcers and\/or warts. While the aim of this response is to clear the invading microbes, in many cases these responses are either evaded or cause pathology that impairs barrier integrity and increases <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> access to target cells in the sub\u2010mucosa. In addition, innate responses to <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s can result in an increased number of immune cells, including those that are the primary targets of <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>, and may contribute to the association between <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s and increased susceptibility to <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> acquisition. Many of these cells are mediators of adaptive immunity, including tissue\u2010resident cells that may also display innate\u2010like functions. Bacterial vaginosis (<jats:styled-content style=\"fixed-case\">BV<\/jats:styled-content>) is another common cause of inflammation, and evidence for multiple interactions between <jats:styled-content style=\"fixed-case\">BV<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> STI<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> suggest that susceptibility to these conditions should be considered in concert.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s and other microbes can induce inflammation in the genital tract, perturbing the normal robust function of the mucosal barrier against <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content>. While the impact of <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s on the mucosal immune system and <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> acquisition is often under\u2010appreciated, understanding their interactions of the infections with the immune responses play an important role in improving treatment and reducing the risk of <jats:styled-content style=\"fixed-case\">HIV<\/jats:styled-content> acquisition. The frequent sub\u2010clinical inflammation associated with <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content>s underscores the need for better <jats:styled-content style=\"fixed-case\">STI<\/jats:styled-content> diagnostics to reverse the immunological consequences of infection.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jia2.25346","type":"journal-article","created":{"date-parts":[[2019,8,30]],"date-time":"2019-08-30T07:02:14Z","timestamp":1567148534000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":70,"title":["Mechanisms of sexually transmitted infection\u2010induced inflammation in women: implications for <scp>HIV<\/scp> risk"],"prefix":"10.1002","volume":"22","author":[{"given":"Ruth","family":"Mwatelah","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology and Infectious Diseases University of Manitoba Winnipeg Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lyle R","family":"McKinnon","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology and Infectious Diseases University of Manitoba Winnipeg Canada"},{"name":"Centre for the AIDS Programme of Research in South Africa (CAPRISA) University of KwaZulu\u2010Natal Durban South Africa"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheryl","family":"Baxter","sequence":"additional","affiliation":[{"name":"Centre for the AIDS Programme of Research in South Africa (CAPRISA) University of KwaZulu\u2010Natal Durban South Africa"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quarraisha","family":"Abdool Karim","sequence":"additional","affiliation":[{"name":"Centre for the AIDS Programme of Research in South Africa (CAPRISA) University of KwaZulu\u2010Natal Durban South Africa"},{"name":"Department of Epidemiology Columbia University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Salim S","family":"Abdool Karim","sequence":"additional","affiliation":[{"name":"Centre for the AIDS Programme of Research in South Africa (CAPRISA) University of KwaZulu\u2010Natal Durban South Africa"},{"name":"Department of Epidemiology Columbia University New York NY USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2019,8,30]]},"reference":[{"key":"e_1_2_7_2_1","unstructured":"WHO.Sexually transmitted infections.Geneva Switzerland:World Health Organisation;2019[cited 2019 Jun 1]. 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