Heme crystallization in a Chagas disease vector acts as a redox-protective mechanism to allow insect reproduction and parasite infection

dc.creatorFerreira, Caroline M.
dc.creatorStiebler, Renata
dc.creatorSaraiva, Francis M.
dc.creatorLechuga, Guilherme C.
dc.creatorNuno, Ana Beatriz Walter
dc.creatorBourguignon, Saulo C.
dc.creatorGonzalez, Marcelo S.
dc.creatorAzambuja, Patricia
dc.creatorGandara, Ana Caroline P.
dc.creatorMenna-Barreto, Rubem F. S.
dc.creatorPaiva-Silva, Gabriela O.
dc.creatorPaes, Marcia C.
dc.creatorOliveira, Marcus F.
dc.date2018-10-09T11:06:50Z
dc.date2018-10-09T11:06:50Z
dc.date2018
dc.date.accessioned2023-09-26T20:18:35Z
dc.date.available2023-09-26T20:18:35Z
dc.identifierFERREIRA, Caroline M. et al. Heme crystallization in a Chagas disease vector acts as a redox-protective mechanism to allow insect reproduction and parasite infection. PLoS Negl Trop Dis., v.12, n.7, e0006661, 20p, July 2018.
dc.identifier1935-2727
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/29448
dc.identifier10.1371/journal.pntd.0006661
dc.identifier1935-2735
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8853892
dc.descriptionHeme crystallization as hemozoin represents the dominant mechanism of heme disposal in blood feeding triatomine insect vectors of the Chagas disease. The absence of drugs or vaccine for the Chagas disease causative agent, the parasite Trypanosoma cruzi, makes the control of vector population the best available strategy to limit disease spread. Although heme and redox homeostasis regulation is critical for both triatomine insects and T. cruzi, the physiological relevance of hemozoin for these organisms remains unknown. Here, we demonstrate that selective blockage of heme crystallization in vivo by the antimalarial drug quinidine, caused systemic heme overload and redox imbalance in distinct insect tissues, assessed by spectrophotometry and fluorescence microscopy. Quinidine treatment activated compensatory defensive heme-scavenging mechanisms to cope with excessive heme, as revealed by biochemical hemolymph analyses, and fat body gene expression. Importantly, egg production, oviposition, and total T. cruzi parasite counts in R. prolixus were significantly reduced by quinidine treatment. These effects were reverted by oral supplementation with the major insect antioxidant urate. Altogether, these data underscore the importance of heme crystallization as the main redox regulator for triatomine vectors, indicating the dual role of hemozoin as a protective mechanism to allow insect fertility, and T. cruzi life-cycle. Thus, targeting heme crystallization in insect vectors represents an innovative way for Chagas disease control, by reducing simultaneously triatomine reproduction and T. cruzi transmission.
dc.formatapplication/pdf
dc.languageeng
dc.publisherPublic Library of Science
dc.rightsopen access
dc.subjectDoença de Chagas
dc.subjectcristalização do heme
dc.subjectvetor
dc.subjectmecanismo de proteção redox
dc.subjecteprodução de insetos
dc.subjectinfecção por parasitas
dc.subjectChagas Disease
dc.subjectHeme crystallization
dc.subjectredox-protective mechanism
dc.subjectinsect reproduction
dc.subjectparasite infection
dc.subjectvector
dc.titleHeme crystallization in a Chagas disease vector acts as a redox-protective mechanism to allow insect reproduction and parasite infection
dc.typeArticle


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