Molecular mechanisms of host cell invasion by Trypanosoma cruzi

Conrad L. Epting; Bria M. Coates; David M. Engman

doi:10.1016/j.exppara.2010.06.023

Molecular mechanisms of host cell invasion by Trypanosoma cruzi

Conrad L. Epting^*, Bria M. Coates, David M. Engman

^*Corresponding author for this work

Pediatrics

Research output: Contribution to journal › Article › peer-review

73 Scopus citations

Abstract

The protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, is an obligate intracellular protozoan pathogen. Overlapping mechanisms ensure successful infection, yet the relationship between these cellular events and clinical disease remains obscure. This review explores the process of cell invasion from the perspective of cell surface interactions, intracellular signaling, modulation of the host cytoskeleton and endosomal compartment, and the intracellular innate immune response to infection.

Original language	English (US)
Pages (from-to)	283-291
Number of pages	9
Journal	Experimental Parasitology
Volume	126
Issue number	3
DOIs	https://doi.org/10.1016/j.exppara.2010.06.023
State	Published - Nov 2010

Funding

We are grateful to Cheryl L Olson for the photomicrographs provided for this review. CLE and DME were supported in part by Grants from the United States National Institutes of Health .

Keywords

Invasion
Lysosome
Microtubules
Signaling
Trypanosoma cruzi

ASJC Scopus subject areas

Infectious Diseases
Parasitology
Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.exppara.2010.06.023

Cite this

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title = "Molecular mechanisms of host cell invasion by Trypanosoma cruzi",

abstract = "The protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, is an obligate intracellular protozoan pathogen. Overlapping mechanisms ensure successful infection, yet the relationship between these cellular events and clinical disease remains obscure. This review explores the process of cell invasion from the perspective of cell surface interactions, intracellular signaling, modulation of the host cytoskeleton and endosomal compartment, and the intracellular innate immune response to infection.",

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author = "Epting, {Conrad L.} and Coates, {Bria M.} and Engman, {David M.}",

note = "Funding Information: We are grateful to Cheryl L Olson for the photomicrographs provided for this review. CLE and DME were supported in part by Grants from the United States National Institutes of Health .",

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AU - Epting, Conrad L.

AU - Coates, Bria M.

AU - Engman, David M.

N1 - Funding Information: We are grateful to Cheryl L Olson for the photomicrographs provided for this review. CLE and DME were supported in part by Grants from the United States National Institutes of Health .

PY - 2010/11

Y1 - 2010/11

N2 - The protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, is an obligate intracellular protozoan pathogen. Overlapping mechanisms ensure successful infection, yet the relationship between these cellular events and clinical disease remains obscure. This review explores the process of cell invasion from the perspective of cell surface interactions, intracellular signaling, modulation of the host cytoskeleton and endosomal compartment, and the intracellular innate immune response to infection.

AB - The protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, is an obligate intracellular protozoan pathogen. Overlapping mechanisms ensure successful infection, yet the relationship between these cellular events and clinical disease remains obscure. This review explores the process of cell invasion from the perspective of cell surface interactions, intracellular signaling, modulation of the host cytoskeleton and endosomal compartment, and the intracellular innate immune response to infection.

KW - Invasion

KW - Lysosome

KW - Microtubules

KW - Signaling

KW - Trypanosoma cruzi

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Molecular mechanisms of host cell invasion by Trypanosoma cruzi

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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