Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 74, Issue 5, Pages 868-879Publisher
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.0303116
Keywords
lipid mediators; inflammation; bone marrow-derived dendritic cells; chemokines
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Funding
- NIAID NIH HHS [AI052306, AI47325] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI052306, R01AI147325, R01AI047325, R56AI047325] Funding Source: NIH RePORTER
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Dendritic cells bridge innate and adaptive immunity and participate in both responses. Upon capture of pathogens, dendritic cells release inflammatory cytokines and chemokines, attracting other immune cells to the infection site. Antiinflammatory cytokines, glucocorticoids, anti-inflammatory neuropeptides, and lipid mediators such as prostaglandin E2 (PGE(2)) limit and control the inflammatory response. In this study we report that exogenous PGE(2) inhibits CCL3 (MIP-1alpha) and CCL4 (MIP-1beta) expression and release from dendritic cells stimulated with either lipopolysaccharide (LPS), a TLR4 ligand, or peptidoglycan, a TLR2 ligand. The inhibition is dose-dependent and occurs at both the mRNA and protein levels. The inhibitory effect is mediated through EP2 and EP4 receptors and requires the presence of PGE(2) at the time of LPS stimulation. Intraperitoneal administration of PGE(2) together with LPS results in a reduction in the levels of CCL3 and CCL4 released in the peritoneal fluid, a reduction in the number of dendritic cells accumulating in the peritoneal cavity, and a reduction in CCL3 amount per cell in the peritoneal cell population. These results suggest that one of the mechanisms by which endogenous PGE(2) acts as an anti-inflammatory agent, is the inhibition of inflammatory chemokine release from activated dendritic cells, preventing the excess accumulation of activated immune cells.
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