Internalization of a non-pathogenic mycobacteria by macropinocytosis in human alveolar epithelial A549 cells

Blanca Estela García-Pérez, Juan Carlos Hernández-González, Samuel García-Nieto, Julieta Luna-Herrera

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Mycobacterium smegmatis (MSM) a non-pathogenic mycobacterium is often employed as a tool to understand many aspects of the mycobacterial infections. However, its own biology and particularly its mechanism of entry into non-phagocytic cells are not well known. Previously, we demonstrated that Mycobacterium tuberculosis (MTB) invades epithelial cells by macropinocytosis. In the present study, we investigated whether MSM also invades human epithelial type II pneumocytes (A549) by macropinocytosis. Infection of A549 cells with MSM elicited actin filaments redistribution, lamellipodia formation and increased fluid phase uptake, suggesting macropinocytosis. Furthermore, macropinocytosis inhibitors like cytochalasin D and amiloride caused inhibition of fluid phase and bacterial uptake. We can conclude that MSM, like MTB, takes advantage of macropinocytosis for entry into epithelial cells, however, unlike MTB, internalized MSM are killed by host cells. These findings suggest that induction of macropinocytosis and cell invasion is not an exclusive feature of pathogenic organisms. © 2008 Elsevier Ltd. All rights reserved.
Original languageAmerican English
Pages (from-to)1-6
Number of pages0
JournalMicrobial Pathogenesis
DOIs
StatePublished - 1 Jul 2008

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Mycobacterium smegmatis
Alveolar Epithelial Cells
Mycobacterium
Mycobacterium tuberculosis
Epithelial Cells
Cytochalasin D
Pseudopodia
Amiloride
Infection
Actin Cytoskeleton
A549 Cells

Cite this

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title = "Internalization of a non-pathogenic mycobacteria by macropinocytosis in human alveolar epithelial A549 cells",
abstract = "Mycobacterium smegmatis (MSM) a non-pathogenic mycobacterium is often employed as a tool to understand many aspects of the mycobacterial infections. However, its own biology and particularly its mechanism of entry into non-phagocytic cells are not well known. Previously, we demonstrated that Mycobacterium tuberculosis (MTB) invades epithelial cells by macropinocytosis. In the present study, we investigated whether MSM also invades human epithelial type II pneumocytes (A549) by macropinocytosis. Infection of A549 cells with MSM elicited actin filaments redistribution, lamellipodia formation and increased fluid phase uptake, suggesting macropinocytosis. Furthermore, macropinocytosis inhibitors like cytochalasin D and amiloride caused inhibition of fluid phase and bacterial uptake. We can conclude that MSM, like MTB, takes advantage of macropinocytosis for entry into epithelial cells, however, unlike MTB, internalized MSM are killed by host cells. These findings suggest that induction of macropinocytosis and cell invasion is not an exclusive feature of pathogenic organisms. {\circledC} 2008 Elsevier Ltd. All rights reserved.",
author = "Garc{\'i}a-P{\'e}rez, {Blanca Estela} and Hern{\'a}ndez-Gonz{\'a}lez, {Juan Carlos} and Samuel Garc{\'i}a-Nieto and Julieta Luna-Herrera",
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Internalization of a non-pathogenic mycobacteria by macropinocytosis in human alveolar epithelial A549 cells. / García-Pérez, Blanca Estela; Hernández-González, Juan Carlos; García-Nieto, Samuel; Luna-Herrera, Julieta.

In: Microbial Pathogenesis, 01.07.2008, p. 1-6.

Research output: Contribution to journalArticle

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N2 - Mycobacterium smegmatis (MSM) a non-pathogenic mycobacterium is often employed as a tool to understand many aspects of the mycobacterial infections. However, its own biology and particularly its mechanism of entry into non-phagocytic cells are not well known. Previously, we demonstrated that Mycobacterium tuberculosis (MTB) invades epithelial cells by macropinocytosis. In the present study, we investigated whether MSM also invades human epithelial type II pneumocytes (A549) by macropinocytosis. Infection of A549 cells with MSM elicited actin filaments redistribution, lamellipodia formation and increased fluid phase uptake, suggesting macropinocytosis. Furthermore, macropinocytosis inhibitors like cytochalasin D and amiloride caused inhibition of fluid phase and bacterial uptake. We can conclude that MSM, like MTB, takes advantage of macropinocytosis for entry into epithelial cells, however, unlike MTB, internalized MSM are killed by host cells. These findings suggest that induction of macropinocytosis and cell invasion is not an exclusive feature of pathogenic organisms. © 2008 Elsevier Ltd. All rights reserved.

AB - Mycobacterium smegmatis (MSM) a non-pathogenic mycobacterium is often employed as a tool to understand many aspects of the mycobacterial infections. However, its own biology and particularly its mechanism of entry into non-phagocytic cells are not well known. Previously, we demonstrated that Mycobacterium tuberculosis (MTB) invades epithelial cells by macropinocytosis. In the present study, we investigated whether MSM also invades human epithelial type II pneumocytes (A549) by macropinocytosis. Infection of A549 cells with MSM elicited actin filaments redistribution, lamellipodia formation and increased fluid phase uptake, suggesting macropinocytosis. Furthermore, macropinocytosis inhibitors like cytochalasin D and amiloride caused inhibition of fluid phase and bacterial uptake. We can conclude that MSM, like MTB, takes advantage of macropinocytosis for entry into epithelial cells, however, unlike MTB, internalized MSM are killed by host cells. These findings suggest that induction of macropinocytosis and cell invasion is not an exclusive feature of pathogenic organisms. © 2008 Elsevier Ltd. All rights reserved.

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