Hijacking of macrophages by Salmonella (3, 10: r: -) through ‘types-III’ secretion-like exocytotic signaling: a mechanism for infection in chicken ileum

Ultrastructural studies of experimentally-infected chicken ileum reveal that virulent Salmonellae (3, 10: r: -) signal their own phagocytosis by tissue macrophages, and are thus able to dodge host defence mechanisms. The observed fusion of membrane vesicles (MVs) liberated from virulent organisms with closely interacting macrophages is proposed here to constitute a mechanism for type ill secretion-like system of gram-negative organisms in general, in order to translocate the necessary biochemical signals into the cytosol of macrophages (eucaryotic host cells). This leads to (i) membrane ruftling culminating in augmented phagocytosis of salmonellae, (ii)inhibition of phagosome-lysosome (P-L) fusion for survival and replication of the pathogens within thehost cytoplasm and (iii) initiation of apoptosis of the infected macrophages and ultimate release of salmonellae from the migrating host cells.