Histamine Regulation of Interleukin-18-Initiating Cytokine Cascade Is Associated with Down-Regulation of Intercellular Adhesion Molecule-1 Expression in Human Peripheral Blood Mononuclear Cells

Abstract

In the previous study, we demonstrated that interleukin (IL)-18 up-regulated intercellular adhesion molecule-1 (ICAM-1) expression on monocytes in human peripheral blood mononuclear cells (PBMC) and that heterotypic interaction between monocytes/T or NK cells through ICAM-1/LFA-1 intensified the production of IL-12, interferon-␥ (IFN-␥), and tumor necrosis factor-␣ (TNF-␣) in PBMC. In the present study, we demonstrate that histamine inhibited the ICAM-1 expression in monocytes induced by IL-18 using flow cytometry and that the responses of IL-12, IFN-␥, and TNF-␣ induced by IL-18 were concentration dependently inhibited by coexisting histamine, whereas IL-18-inhibited IL-10 production was reversed by the same concentrations of histamine. The modulatory effects of histamine on ICAM-1 expression and cytokine production were

Interleukin‐18 enhances monocyte tumor necrosis factor α and interleukin‐1β production induced by direct contact with T lymphocytes: Implications in rheumatoid arthritis

“…In the present study, we found that IL-18, a proinflammatory cytokine associated with various pathologic conditions including RA, dose-dependently enhanced the ability of RA synovial T cells or PHA-prestimulated T lymphocytes to induce production of TNF␣ and IL-1␤, but not IL-10, from resting monocytes upon direct cell-cell contact. Recently, Takahashi et al (25) reported that IL-18 inhibited IL-10 production in cultured PBMCs.…”

Prostaglandin E2 Inhibits IL-18-Induced ICAM-1 and B7.2 Expression Through EP2/EP4 Receptors in Human Peripheral Blood Mononuclear Cells

“…B7.1 and B7.2 have different affinities for their binding partners on T cells, CD28 and CTLA-4, and the differential roles of B7.1 and B7.2 have been suggested for the initial, sustained T cell activation or termination of T cell activation (20,21). Previously, we demonstrated that histamine regulated the IL-18-initiating cytokine cascade through down-regulation of ICAM-1 expression on monocytes (23). The changes may result in a shift of Th1/Th2 balance toward Th2 dominance (23,24).…”

“…Previously, we demonstrated that histamine regulated the IL-18-initiating cytokine cascade through down-regulation of ICAM-1 expression on monocytes (23). The changes may result in a shift of Th1/Th2 balance toward Th2 dominance (23,24). Thus, many kinds of chemical mediators in inflammation may modulate immune responses by regulation of the expression of adhesion molecules.…”

“…The actions of PGE 2 are expected to be exerted via stimulation of the four PGE 2 receptor subtypes, EP1, EP2, EP3, and EP4, alone or in combination. EP1 and EP3 are coupled to a G q protein, phosphatidylinositol production, and increased intracellular Ca 2ϩ concentration (23). EP2 and EP4 are coupled to a G s protein, adenylyl cyclase activation, and cAMP production (26).…”

Natural killer cells in the airways: Do they matter?

“…Moreover, the action of histamine on NK cell function has recently gained attention, providing a potential link between a key factor in allergic asthma and NK cells. Histamine interferes with ICAM-1/LFA-1-dependent cytokine production in monocyte/NK-cell and T-cell cocultures (20) and protects NK cells against apoptosis induced by oxygen radicals (21).…”