alpha-cyclodextrin and Escherichia-coli-Infections

Prostaglandin E series (PGEs) are known to protect against lipopolysaccharide (LPS)-induced liver injury by down-regulating the production of inflammatory cytokines. We show here a novel mechanism whereby prostaglandin E(1) protects mice against liver injury after Escherichia coli infection. Prostaglandin E(1) administration suppressed circulating interleukin 12 (IL-12) levels but increased the IL-10 production after E. coli challenge. Furthermore, prostaglandin E(1)-alpha-cyclodextrin (PGE(1)) shifted the Th1/Th2 balance of CD3(intermediate) IL-2Rbeta(+) T cells in the liver to a dominant Th2-like response. Neutralization of endogenous IL-4 by administration of anti-IL-4 monoclonal antibody (mAb) diminished the inhibitory effect of prostaglandin E(1) on liver injury after E. coli challenge. These results suggested that the Th2-like response of liver T cells may be at least partly involved in the mechanism whereby prostaglandin E(1) protects against E. coli-induced liver injury.

Topics: alpha-Cyclodextrins; Alprostadil; Animals; Antibodies, Monoclonal; Cyclodextrins; Dose-Response Relationship, Drug; Escherichia coli Infections; Female; Interferon-gamma; Interleukin-10; Interleukin-12; Interleukin-4; Killer Cells, Natural; Liver; Liver Diseases; Lymphocyte Count; Mice; Mice, Inbred C3H; RNA, Messenger; T-Lymphocytes; Th2 Cells; Time Factors; Tumor Necrosis Factor-alpha