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In this study, we show that T. cruzi\u2013induced IFN-\u03b2 production was nearly abolished in primary murine cGAS\u2212\/\u2212 or stimulator of IFN genes (STING)-deficient (STINGGt) macrophages and fibroblasts. T. cruzi infection did not impact the ability of IFN-regulatory factor reporter macrophages to respond to classical cGAS\u2013STING agonists, indicating that the limited IFN-\u03b2 induction is not due to active parasite suppression. cGAS\u2212\/\u2212, STINGGt, and IFN-\u03b1\/\u03b2 receptor\u2212\/\u2212 (IFNAR\u2212\/\u2212) macrophages infected with T. cruzi yielded significantly higher numbers of amastigotes compared with wild-type macrophages; however, the impact of the STING pathway during infection in vivo is more complex. Despite an initial increase in parasite growth, STINGGt and IFNAR\u2212\/\u2212 mice ultimately had lower parasite burden in footpads as compared with wild-type mice, demonstrating a role for IFN-I expression in potentiating parasite growth at the infection site. STING pathway activation had little impact on parasite levels in the skeletal muscle; however, in the heart, cGAS\u2212\/\u2212 and STINGGt mice, but not IFNAR\u2212\/\u2212 mice, accumulated higher acute parasite loads, suggesting a protective role of STING sensing of T. cruzi in this organ that was independent of IFN-I. Together, these results demonstrate that host cGAS\u2013STING senses T. cruzi infection, enhancing parasite growth at the site of entry, and contributes to acute-phase parasite restriction in the heart, a major site of tissue damage in chronic T. cruzi infection.<\/jats:p>","DOI":"10.4049\/jimmunol.2300373","type":"journal-article","created":{"date-parts":[[2023,8,21]],"date-time":"2023-08-21T14:37:25Z","timestamp":1692628645000},"page":"1123-1133","source":"Crossref","is-referenced-by-count":7,"title":["cGAS\u2013STING Pathway Activation during <i>Trypanosoma cruzi<\/i> Infection Leads to Tissue-Dependent Parasite Control"],"prefix":"10.1093","volume":"211","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9693-1103","authenticated-orcid":false,"given":"Natasha","family":"Perumal","sequence":"first","affiliation":[{"name":"Center for Tropical and Emerging Global Diseases, University of Georgia , Athens, GA"},{"name":"Department of Cellular Biology, University of Georgia , Athens, GA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0441-1355","authenticated-orcid":false,"given":"Brooke","family":"White","sequence":"additional","affiliation":[{"name":"Center for Tropical and Emerging Global Diseases, University of Georgia , Athens, GA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando","family":"Sanchez-Valdez","sequence":"additional","affiliation":[{"name":"Center for Tropical and Emerging Global Diseases, University of Georgia , Athens, GA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9589-5243","authenticated-orcid":false,"given":"Rick L","family":"Tarleton","sequence":"additional","affiliation":[{"name":"Center for Tropical and Emerging Global Diseases, University of Georgia , Athens, GA"},{"name":"Department of Cellular Biology, University of Georgia , Athens, GA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,8,21]]},"reference":[{"key":"2025020406133122200_r1","doi-asserted-by":"crossref","first-page":"3791","DOI":"10.4049\/jimmunol.1602000","article-title":"Innate control of adaptive immunity: beyond the three-signal paradigm","volume":"198","author":"Jain","year":"2017","journal-title":"J. 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