Avoidance of antimicrobial mechanisms of phagocytic cells

Organisms may secrete toxins which repel or kill the phagocytes. Capsules of carbohydrate (Str. pneumoniae) or polypeptide (Bacillus anthracis) may impede complement deposition and phagocytosis. The M proteins of group A streptococci limit uptake by phagocytes, while permitting specific attachment to the epithelium of the oropharynx. Other organisms are taken up, but fail to trigger the oxidative burst. Secretion of polyanions or ammonia have been reported to block phagolysosome fusion, although the methods used to demonstrate these phenomena have recently been re-evaluated. Superoxide dismu-tase and catalase can degrade oxygen intermediates, and the phenolic glycolipid secreted by M. leprae may act as a scavenger of oxygen radicals. The lipoarabinomannan released from mycobacteria may inhibit lymphokine-mediated macrophage activation, as murine macrophages heavily infected with M. leprae cannot be activated to kill a protozoan. Other organisms avoid antimicrobial mechanisms by escaping from the phagosome. M. leprae and Shigella flexneri can multiply free in the cytoplasm, while Brucella abortus and Legionella pneumophila are found in the rough endoplasmic reticulum.

It is increasingly apparent that many bacteria, like viruses, hijack cellular machinery for their own use. Listeria monocytogenes uses 'hemolysins' to lyse the phagosome, and then interacts with actin in the cell in order to propel itself towards and into neighbouring cells. Finally, some organisms, such as M. tuberculosis tend to kill the macrophage, perhaps by rendering them sensitive to the TNFa which they themselves are induced to release.

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