| Research Abstract |
Phagocytosis, cytokine production and chemotaxis are the major function carried out by neutrophils in an acute inflammation. Infiltrating neutrophils soon undergo in the most part apoptosis with cessation of an acute phase of inflammation. The present study was attempted to investigate how phagocytosis of neutrophils causes effects on their function such as apoptosis, cytokine production and chemotaxis.
Rat neutrophils were separated from cells exudated in the peritoneal cavity after injection of proteosepeptone. Apoptosis was evaluated by fragmentation of DNA and morpholpgy of neutrophilic nuclei. Phagocytosis was brought about by ingestion of oil particles. TNF-α and active oxygen species from neutrophils were determined by a sandwich ELISA and a fluorometric assay, respectively. Apoptosis of neutrophils was inhibited dose-dependently by treatment with a bacterial product, lipopolysaccharide (LPS) or an inflammatory cytokine, IL-1β. This inhibitory effect on apoptosis of neutrophils w
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as abrogated by their ingestion of oil particles. The ingestion of oil particles suppresed a LPS-induced production of TNF-α and reactive oxygen species from neutrophils. Chemotactic activity of neutrophils in response to zymosan-treated serum was assayed in a Boyden chamber. When neutrophils were placed onto an upper chamber with LPS, their chemotactic activity was greatly inhibited. This was reverted to a control level by ingestion of oil particles.
In summary I have shown that phagocytosis of neutrophils diminished a known function of their own induced by either LPS or IL-1β such as suppressed apoptotic propensity, increased cytokine production and altered chemotactic activity. Results suggest that phagocytosis of neutrophils emerging after an early phase of infection may help rescue surrounding normal tissues from a self-destructive nature of purulent inflammation by facilitating their apoptosis, inhibiting production of cytokine and active oxygen species, and by suppressing chemotactic activity. Less
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