Abstract
In this study, chemotactic activity of heat-killed K. pneumoniae DT-S and lipopolysaccharide (LPS), capsular polysaccharide (CPS) of this strain were investigated in mice pleurisy model. Intrapleural inoculation of heat-killed K. pneumoniae DT-S in carrageenan pretreated mice caused more significant neutrophil accumulation than in control mice. This amplified neutrophil accumulation in carrageenan pretreated mice was mainly induced by LPS of heat-killed K. pneumoniae DT-S. Carrageenan pretreated pleural macrophages produced more marked interleukin-1 (IL-1) than control pleural macrophages when stimulated with LPS of K. pneumoniae DT-S. In contrast, CPS induced little IL-1 production even in carrageenan pretreated pleural macrophages and this IL-1 production may be induced by LPS contaminated in CPS of K. pneumoniae DT-S, because polymyxin-B treatment completely inhibited this IL-1 production of CPS in carrageenan pretreated pleural macrophages. Interestingly, there were no IL-1 inducing effects on CPS of K. pneumoniae DT-S in control pleural macrophages.
The results of this study indicated that carrageenan, usually known as antimacrophage agents, caused pleural macrophages to secrete marked IL-1 after stimulation with LPS of K. pneumoniae DT-S. It is considered that this amplified IL-1 production of carrageenan pretreated pleural macrophages in response to LPS, not to CPS, play an important role in neutrophil accumulation on K. pneumoniae DT-S infection.
