ArticlePLoS neglected tropical diseases2011
Trypanosoma cruzi utilizes the host low density lipoprotein receptor in invasion.
Article in PLoS neglected tropical diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 83 citations in OpenAlex.
- Adipose Tissue in Chagas Disease: A Neglected Component of Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- A conserved interaction between the effector Sca4 and host clathrin suggests additional contributions for Sca4 during rickettsial infection.Infection and immunity · 2024Article
- The intersection of hostMicrobiology and molecular biology reviews : MMBR · 2024Review
- Paracrine Signaling Mediated by the Cytosolic Tryparedoxin Peroxidase ofPathogens (Basel, Switzerland) · 2024Article
- Renal protein reabsorption impairment related to a myxosporean infection in the grass frog (Rana temporaria L.).Parasitology research · 2023Article
- Protective effects of Theracurmin treatment during experimental infection of the Colombian strain ofFrontiers in cellular and infection microbiology · 2023Article
- Chromosomal assembly of the flat oyster (Evolutionary applications · 2022Article
- Resveratrol and Curcumin for Chagas Disease Treatment-A Systematic Review.Pharmaceuticals (Basel, Switzerland) · 2022Review
- The Screen of a Phage Display Library Identifies a Peptide That Binds to the Surface ofFrontiers in microbiology · 2022Article
- The Liver and the Hepatic Immune Response inPathogens (Basel, Switzerland) · 2021Review
- Sialic acid removal by trans-sialidase modulates MMP-2 activity during Trypanosoma cruzi infection.Biochimie · 2021Article
- Mechanisms Associated withLife (Basel, Switzerland) · 2021Review
- The response of adipose tissues to Mycoplasma pulmonis and Sendai virus infection in C57BL/6 and DBA/2 mice.The Journal of veterinary medical science · 2021Article
- Symbiotic bracovirus of a parasite manipulates host lipid metabolism via tachykinin signaling.PLoS pathogens · 2021Article
- Review
- Inhibition of SREBP Improves Cardiac Lipidopathy, Improves Endoplasmic Reticulum Stress, and Modulates Chronic Chagas Cardiomyopathy.Journal of the American Heart Association · 2020Article
- A High-Fat Diet Exacerbates the Course of ExperimentalBioMed research international · 2020Article
- Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice.Scientific reports · 2019Article
- Article
- Diet Alters Serum Metabolomic Profiling in the Mouse Model of Chronic Chagas Cardiomyopathy.Disease markers · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundTrypanosoma cruzi, an intracellular protozoan parasite that infects humans and other mammalian hosts, is the etiologic agent in Chagas disease. This parasite can invade a wide variety of mammalian cells. The mechanism(s) by which T. cruzi invades its host cell is not completely understood. The activation of many signaling receptors during invasion has been reported; however, the exact mechanism by which parasites cross the host cell membrane barrier and trigger fusion of the parasitophorous vacuole with lysosomes is not understood. METHODOLOGY/PRINCIPAL
findingsIn order to explore the role of the Low Density Lipoprotein receptor (LDLr) in T. cruzi invasion, we evaluated LDLr parasite interactions using immunoblot and immunofluorescence (IFA) techniques. These experiments demonstrated that T. cruzi infection increases LDLr levels in infected host cells, inhibition or disruption of LDLr reduces parasite load in infected cells, T. cruzi directly binds recombinant LDLr, and LDLr-dependent T. cruzi invasion requires PIP2/3. qPCR analysis demonstrated a massive increase in LDLr mRNA (8000 fold) in the heart of T. cruzi infected mice, which is observed as early as 15 days after infection. IFA shows a co-localization of both LDL and LDLr with parasites in infected heart. CONCLUSIONS/SIGNIFICANCE: These data highlight, for the first time, that LDLr is involved in host cell invasion by this parasite and the subsequent fusion of the parasitophorous vacuole with the host cell lysosomal compartment. The model suggested by this study unifies previous models of host cell invasion for this pathogenic protozoon. Overall, these data indicate that T. cruzi targets LDLr and its family members during invasion. Binding to LDL likely facilitates parasite entry into host cells. The observations in this report suggest that therapeutic strategies based on the interaction of T. cruzi and the LDLr pathway should be pursued as possible targets to modify the pathogenesis of disease following infection.
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