Pathogen-induced apoptosis of macrophages: a common end for different pathogenic strategies
Article first published online: 24 DEC 2001
Volume 2, Issue 4, pages 265–273, August 2000
How to Cite
Navarre, W. W. and Zychlinsky, A. (2000), Pathogen-induced apoptosis of macrophages: a common end for different pathogenic strategies. Cellular Microbiology, 2: 265–273. doi: 10.1046/j.1462-5822.2000.00056.x
- Issue published online: 24 DEC 2001
- Article first published online: 24 DEC 2001
- Received 2 February, 2000; revised 1 April, 2000; accepted 12 April, 2000.
Microbe–macrophage interactions play a central role in the pathogenesis of many infections. Several bacterial pathogens induce apoptosis specifically in macrophages, but the mechanisms by which it occurs differ, and the resulting pathology can take different courses. Macrophage death caused by Shigella flexneri and Salmonella spp. has been shown to result in the release of pro-inflammatory cytokines. Conversely, Yersinia spp. induce apoptosis by suppressing the signalling pathways that lead to the production of tumour necrosis factor (TNF)-α, a cytokine essential for the control of this infection. It is likely that there are a variety of reasons why macrophages are particularly susceptible to pathogen-induced apoptosis. One reason may be the expression of surface receptors that recognize highly conserved bacterial components, such as lipopolysaccharide (LPS) and bacterial lipoproteins (BLPs). These receptors have recently been shown to activate pro-apoptotic signalling pathways. The roles of macrophage apoptosis in different disease processes are discussed.