Replies to post #18119 on Avid Bioservices Inc (CDMO)

[jazzbeerman]

TB infected cells: exposed PS -



Survival of Mycobacterium tuberculosis in Host Macrophages Involves Resistance to Apoptosis Dependent upon Induction of Antiapoptotic Bcl-2 Family Member Mcl-11



The Journal of Immunology
http://www.jimmunol.org/cgi/content/full/170/1/430



Introduction

Mycobacterium tuberculosis, the causative agent of pulmonary tuberculosis, infects one-third of the world’s population (1). It accounts for more deaths each year than any other single infectious bacteria (2). Its ability to survive and replicate in the host macrophage is critical to its pathogenesis, emphasizing a need for a clearer understanding of its interactions with the host macrophage. In vitro experimental models have demonstrated that M. tuberculosis infection causes apoptosis of host macrophages. This has been demonstrated by the detection of annexin V binding to surface-exposed phosphatidylserine early after infection with M. tuberculosis (3). In vitro infection of human macrophages with M. tuberculosis strain H37Ra or strain H37Rv caused TNF-{alpha}-dependent apoptosis demonstrated by a genomic DNA ladder, nuclear fragmentation, and condensation as well as by TUNEL labeling (4). Keane et al. (5) demonstrated further that avirulent M. tuberculosis strains and Mycobacterium bovis bacillus Calmette-Guérin (BCG)4 cause more apoptosis than virulent strains, implicating a role for apoptosis in host defense against M. tuberculosis.




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Evolution has favored pathogenesis that resembles apoptosis.


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