PMID- 8656050 OWN - NLM STAT- MEDLINE DCOM- 19960801 LR - 20190516 IS - 0741-5400 (Print) IS - 0741-5400 (Linking) VI - 59 IP - 5 DP - 1996 May TI - Integrin-mediated epithelial-T cell interaction enhances nitric oxide production and increased intracellular inhibition of Chlamydia. PG - 656-62 AB - T cell-mediated immunity against Chlamydia in mice is mediated at least in part by T cell-derived interferon-gamma (IFN-gamma) induction of the nitric oxide synthase (iNOS) system in infected epithelial cells. Although IFN-gamma alone could stimulate nitric oxide (NO) production from epithelial cells and inhibit the intracellular growth of Chlamydia, the effectiveness was less than when infected epithelial cells were co-cultured with IFN-gamma-producing T cell clones. In co-cultures containing T cells and infected epithelial cells, additional NO produced by activated T cells could augment chlamydial killing; however, T cell-derived NO was insufficient to account for the total NO present in the co-culture and therefore could not explain the dramatic increase in chlamydial inhibition under those conditions. To determine whether direct cell-to-cell interaction involving adhesion molecules was involved in increased NO induction, the ability of neutralizing monoclonal antibodies directed against intercellular adhesion molecule type 1 (ICAM-1) and leukocyte function antigen-1 (LFA-1) to suppress NO production and lower intracellular chlamydial inhibition was investigated. It was found that monoclonal antibodies against ICAM-1/LFA-1 could significantly reduce the capacity of a protective CD4+ type 1 (Thl) clone (clone 2.14-0) to inhibit the intracellular growth of the C. trachomatis agent of mouse pneumonitis (MoPn). The suppression of the anti-chlamydial action of the clone by antibodies correlated with approximately 50% decrease in NO production. Also, paraformaldehyde-fixed clone 2.14-0 could enhance NO induction and chlamydial inhibition mediated by IFN-gamma, and this effect could be reversed by anti-ICAM-1/LFA-1 antibodies. The results indicated that epithelial-T cell interaction via adhesion molecules enhances NO production and increased chlamydial inhibition by IFN-gamma-secreting T cells. FAU - Igietseme, J U AU - Igietseme JU AD - Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock 72205, USA. FAU - Uriri, I M AU - Uriri IM FAU - Hawkins, R AU - Hawkins R FAU - Rank, R G AU - Rank RG LA - eng GR - AI26328/AI/NIAID NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - England TA - J Leukoc Biol JT - Journal of leukocyte biology JID - 8405628 RN - 0 (Integrins) RN - 0 (Lymphocyte Function-Associated Antigen-1) RN - 31C4KY9ESH (Nitric Oxide) RN - 82115-62-6 (Interferon-gamma) SB - IM MH - Animals MH - Cell Communication MH - Cells, Cultured MH - Chlamydia/*immunology MH - Coculture Techniques MH - Epithelial Cells MH - Female MH - Integrins/*physiology MH - Interferon-gamma/pharmacology MH - Lymphocyte Function-Associated Antigen-1/physiology MH - Mice MH - Mice, Inbred BALB C MH - Nitric Oxide/*biosynthesis MH - T-Lymphocytes/*physiology EDAT- 1996/05/01 00:00 MHDA- 1996/05/01 00:01 CRDT- 1996/05/01 00:00 PHST- 1996/05/01 00:00 [pubmed] PHST- 1996/05/01 00:01 [medline] PHST- 1996/05/01 00:00 [entrez] AID - 10.1002/jlb.59.5.656 [doi] PST - ppublish SO - J Leukoc Biol. 1996 May;59(5):656-62. doi: 10.1002/jlb.59.5.656.