TY - JOUR
T1 - Internalization of a non-pathogenic mycobacteria by macropinocytosis in human alveolar epithelial A549 cells
AU - García-Pérez, Blanca Estela
AU - Hernández-González, Juan Carlos
AU - García-Nieto, Samuel
AU - Luna-Herrera, Julieta
N1 - Funding Information:
This project was supported by CONACyT SEP-2004-C01-47496 and SIP/IPN project 20070271 and 20070610. BEGP is SNI, COFAA and EDI fellow. SGN was PIFI and CONACyT fellow. JCHG is PIFI and CONACyT fellow. JLH is COFAA, EDI and SNI fellow. Authors acknowledge Electron Microscopy Central of ENCB/IPN for technical assistance. We thank to Dr. V. Reddy for critical reading of this manuscript and Dr R. Coral for technical support on ApoTome system microscopy.
PY - 2008/7
Y1 - 2008/7
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.
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.
KW - Macropinocytosis
KW - Mycobacterium smegmatis
KW - Non-phagocytic cells
KW - Pneumocytes type II
UR - http://www.scopus.com/inward/record.url?scp=44649193792&partnerID=8YFLogxK
U2 - 10.1016/j.micpath.2008.01.009
DO - 10.1016/j.micpath.2008.01.009
M3 - Artículo
SN - 0882-4010
VL - 45
SP - 1
EP - 6
JO - Microbial Pathogenesis
JF - Microbial Pathogenesis
IS - 1
ER -