2023
DOI: 10.3390/jcm12082888
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Genetic Ablation and Pharmacological Blockade of Bradykinin B1 Receptor Unveiled a Detrimental Role for the Kinin System in Chagas Disease Cardiomyopathy

Abstract: Chagas disease, the parasitic infection caused by Trypanosoma cruzi, afflicts about 6 million people in Latin America. Here, we investigated the hypothesis that T. cruzi may fuel heart parasitism by activating B1R, a G protein-coupled (brady) kinin receptor whose expression is upregulated in inflamed tissues. Studies in WT and B1R−/− mice showed that T. cruzi DNA levels (15 days post infection—dpi) were sharply reduced in the transgenic heart. FACS analysis revealed that frequencies of proinflammatory neutroph… Show more

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Cited by 3 publications
(2 citation statements)
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References 67 publications
(131 reference statements)
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“…Thus, the B1R is potentially important in sustained inflammatory states and infectious disease. For instance, treatment with a B1R antagonist decreased mortality and mitigated cardiac inflammation and dysfunction in an experimental Chagas disease model in mice [29]. However, it does not follow that B1R should be systematically blocked in tissue injury situations; for instance, the development of an adaptative collateral circulation is mediated by this receptor subtype following arterial occlusion in a rodent model [30].…”
Section: Kinin Receptorsmentioning
confidence: 99%
“…Thus, the B1R is potentially important in sustained inflammatory states and infectious disease. For instance, treatment with a B1R antagonist decreased mortality and mitigated cardiac inflammation and dysfunction in an experimental Chagas disease model in mice [29]. However, it does not follow that B1R should be systematically blocked in tissue injury situations; for instance, the development of an adaptative collateral circulation is mediated by this receptor subtype following arterial occlusion in a rodent model [30].…”
Section: Kinin Receptorsmentioning
confidence: 99%
“…The contact system serves as the activation starting point for both the intrinsic coagulation pathway and the kallikrein–kinin system (KKS), representing an intimate connection between coagulation and intravascular inflammation [ 6 ]. The prothrombogenic and proinflammatory responses resulting from the converging action of these cascades contribute to the pathogenesis of several infectious diseases caused by intracellular protozoa [ 7 , 8 , 9 , 10 ], yeasts [ 11 ], Gram-positive bacteria [ 12 , 13 ], or viruses [ 14 , 15 ].…”
Section: Introductionmentioning
confidence: 99%