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Infect. Immun. doi:10.1128/IAI.00614-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Bystander macrophage apoptosis after Mycobacterium tuberculosis H37Ra infection

Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin and St. James's Hospital, Dublin, Ireland

^* To whom correspondence should be addressed. Email: jkeane{at}stjames.ie.

	Abstract

Human macrophages infected with Mycobacterium tuberculosis undergo apoptosis. Macrophage apoptosis contributes to the innate immune response against M. tuberculosis by containing and limiting the growth of mycobacteria, and also by depriving the bacillus of its niche cell. Apoptosis of infected macrophages is well documented; however, bystander apoptosis of uninfected macrophages has not been described in the setting of M. tuberculosis (Mtb). We observed that uninfected human macrophages underwent significant bystander apoptosis 48 h and 96 h after being in contact with macrophages infected with avirulent Mtb. Bystander apoptosis was significantly higher than the background apoptosis observed in uninfected control cells cultured for the same length of time. There was no evidence for the involvement of TNF, Fas, TRAIL, TGF, TLR2 or MyD88 in contact mediated bystander apoptosis. This newly described phenomenon may further limit the spread of Mtb by eliminating the niche cells on which the bacillus relies.

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