ArticleMalaria journal2019
Malaria infection promotes a selective expression of kinin receptors in murine liver.
Article in Malaria journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.Bioscience reports · 2024Review
- The des-ArgFrontiers in physiology · 2022Article
- Malaria link of hypertension: a hidden syndicate of angiotensin II, bradykinin and sphingosine 1-phosphate.Human cell · 2021Review
- Differential Effect of Antioxidants Glutathione and Vitamin C on the Hepatic Injuries Induced byBioMed research international · 2021Article
- Polarized Proteins in Endothelium and Their Contribution to Function.Journal of vascular research · 2021Review
- Acute Phase Responses Vary Between Children of HbAS and HbAA Genotypes DuringJournal of inflammation research · 2021Article
- Kinins and Their Receptors in Infectious Diseases.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?Frontiers in immunology · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
backgroundMalaria represents a worldwide medical emergency affecting mainly poor areas. Plasmodium parasites during blood stages can release kinins to the extracellular space after internalization of host kininogen inside erythrocytes and these released peptides could represent an important mechanism in liver pathophysiology by activation of calcium signaling pathway in endothelial cells of vertebrate host. Receptors (B1 and B2) activated by kinins peptides are important elements for the control of haemodynamics in liver and its physiology. The aim of this study was to identify changes in the liver host responses (i.e. kinin receptors expression and localization) and the effect of ACE inhibition during malaria infection using a murine model.
methodsBalb/C mice infected by Plasmodium chabaudi were treated with captopril, an angiotensin I-converting enzyme (ACE) inhibitor, used alone or in association with the anti-malarial chloroquine in order to study the effect of ACE inhibition on mice survival and the activation of liver responses involving B1R and B2R signaling pathways. The kinin receptors (B1R and B2R) expression and localization was analysed in liver by western blotting and immunolocalization in different conditions.
resultsIt was verified that captopril treatment caused host death during the peak of malaria infection (parasitaemia about 45%). B1R expression was stimulated in endothelial cells of sinusoids and other blood vessels of mice liver infected by P. chabaudi. At the same time, it was also demonstrated that B1R knockout mice infected presented a significant reduction of survival. However, the infection did not alter the B2R levels and localization in liver blood vessels.
conclusionsThus, it was observed through in vivo studies that the vasodilation induced by plasma ACE inhibition increases mice mortality during P. chabaudi infection. Besides, it was also seen that the anti-malarial chloroquine causes changes in B1R expression in liver, even after days of parasite clearance. The differential expression of B1R and B2R in liver during malaria infection may have an important role in the disease pathophysiology and represents an issue for clinical treatments.
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