cAMP-increasing agents such as prostaglandin E2 (PGE2) are known to protect against LPS-induced liver injury by downregulating the production of inflammatory cytokines such as TNF-α. However, the effects of such reagents on host defense against bacterial infection remain unknown. We show here that in vivo administration of PGE2 significantly protected mice against liver injury after Escherichia coli infection but hampered the resolution of the infection. PGE2 significantly suppressed circulating TNF-α and IL-12 levels but increased the IL-10 production after E. coli challenge. PGE2 inhibited the emergence of γδ T cells in the peritoneal cavity, which are important for host defense against E. coli, and deteriorated bacterial exclusion in the peritoneal cavity after E. coli challenge. These results suggested that PGE2 affects host defense mechanisms against E. coli infection through modulation of cytokine production and γδ T cell accumulation.
|Number of pages||7|
|Journal||Journal of Immunology|
|Publication status||Published - Sep 15 1998|
All Science Journal Classification (ASJC) codes
- Immunology and Allergy