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In this study, we investigated the effects of acute and chronic\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>T. cruzi<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection on vascular responsiveness and the underlying mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      Male Wistar Hannover rats were infected intraperitoneally with 1\u2009\u00d7\u200910\n                      <jats:sup>5<\/jats:sup>\n                      trypomastigotes of the\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>T. cruzi<\/jats:italic>\n                      <\/jats:styled-content>\n                      Y strain. Vascular function was evaluated in the thoracic aorta during the acute (9\u2009days post\u2010infection, dpi) and chronic (60 dpi) phases of infection.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      No changes in vascular responsiveness were observed during the chronic phase. However, acute\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>T. cruzi<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection induced endothelial dysfunction, leading to vascular hypercontractility, although it did not alter the anti\u2010contractile effect of perivascular adipose tissue (PVAT). Infected rats exhibited increased levels of TNF\u2010\n                      <jats:italic>\u03b1<\/jats:italic>\n                      in the aorta, but not in the PVAT or serum. TNF\u2010\n                      <jats:italic>\u03b1<\/jats:italic>\n                      inhibition with etanercept (1\u2009mg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      \u00b7day\n                      <jats:sup>\u22121<\/jats:sup>\n                      ; i.p.) prevented both endothelial dysfunction and oxidative stress (upregulation of NOX2\/superoxide [O\u2082\u2022\n                      <jats:sup>\u2212<\/jats:sup>\n                      ] generation), as well as the increase in thromboxane A\n                      <jats:sub>2<\/jats:sub>\n                      (TXA\n                      <jats:sub>2<\/jats:sub>\n                      ).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>\n                      Our results demonstrate that TNF\u2010\n                      <jats:italic>\u03b1<\/jats:italic>\n                      mediates vascular dysfunction during the acute phase of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>T. cruzi<\/jats:italic>\n                      <\/jats:styled-content>\n                      infection. Our results indicate that TNF\u2010\n                      <jats:italic>\u03b1<\/jats:italic>\n                      contributes to endothelial dysfunction and vascular hypercontractility by promoting O\u2082\u2022\n                      <jats:sup>\u2212<\/jats:sup>\n                      generation, upregulating NOX2 and increasing TXA\n                      <jats:sub>2<\/jats:sub>\n                      production. Although PVAT is not dysfunctional during acute infection, increased myeloperoxidase (MPO) activity was detected within it, suggesting it may act as a reservoir for neutrophils.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.70322","type":"journal-article","created":{"date-parts":[[2025,12,29]],"date-time":"2025-12-29T01:08:19Z","timestamp":1766970499000},"page":"2256-2272","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["TNF\u2010\n                    <i>\u03b1<\/i>\n                    partially modulates the endothelial dysfunction during the acute phase of\n                    <i>Trypanosoma cruzi<\/i>\n                    infection"],"prefix":"10.1111","volume":"183","author":[{"given":"Thales M. 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