Abstract
To elucidate the mechanism of switching from neutrophils accumulation in the early phase to chronic inflammation characterized by the predominant accumulation of mononuclear cells in tuberculous inflammation, expression of the chemokines was examined. Neutrophils stimulated with lipopolysaccharide (LPS), M. tuberculosis (MT), or purified protein derivative (PPD) expressed both IL-8 and MIP-1α, however, the kinetics of expression did not differ. The viability of neutrophils was much reduced in response to mycobacterial derivatives with TNFα. Apoptosis seemed to cause the low viability of neutrophils, which might rapidly remove neutrophils from tuberculous inflammatory sites.
Monocytes stimulated with M. tuberculosis or PPD expressed IL 8, MIP-1α and MCP 1. The expression of MCP-1 appeared in the later phase than those of IL-8 and MIP-1α. However monocytes stimulated with LPS could not induce production of MCP-1 strongly. These kinetics of chemokines induced in inflammatory cells by tuberculous derivatives may contribute to formation of tuberculous inflammation. In addition killing mycobacterium in macrophages depended on activation of Thl cellsmacrophages response, which was associated with at least partially IL 12 production.
