Histamine‐induced inhibition of neutrophil chemotaxis and T‐lymphocyte proliferation in man

Abstract

Histamine inhibits in vitro human neutrophil chemotaxis and T-lymphocyte proliferation via H2 receptors. The aim of this study was to verify these inhibitory effects of histamine in man in vivo. Healthy volunteers were challenged with histamine by intravenous (1 mg), subcutaneous (1 mg) and inhalatory (2.4 mg) routes. Venous blood was taken before and at different times after challenge. Neutrophil chemotaxis was studied by the Boyden assay and T-lymphocyte proliferation by counting H3-thymidine incorporation in cultured mononuclear cells. Plasma histamine was measured by radioimmunoassay. Histamine infusion caused transient systemic symptoms as well as a significant decrease of neutrophil chemotaxis (mean - 26% +/- 6) and of PHA-pulsed T-lymphocyte proliferation (mean - 16% +/- 6) 4 h after histamine challenge. Subcutaneous injection of histamine caused only a significant decrease of neutrophil chemotaxis (mean - 24% +/- 15) 4 h after injection. Histamine inhalation was well tolerated and caused a significant depression of neutrophil chemotaxis (mean - 40% +/- 15) and of T-lymphocyte proliferation (mean - 27% +/- 6) 2 and 4 h after the challenge. Histamine challenges were always accompanied by a rapid and transient rise in plasma histamine. Inhalation of an H2 agonist (impromidine) but not of an H1 agonist (betahistine) caused a decrease of neutrophil chemotaxis and of T-lymphocyte proliferation. Oral pretreatment with an H2 antagonist (cimetidine) before histamine inhalation prevented histamine-induced decrease of neutrophil chemotaxis and T-lymphocyte proliferation, whereas astemizole, an H1 antagonist, had no effect. In conclusion, during the few hours following administration, exogenous histamine in man causes a depression of neutrophil chemotaxis and T-lymphocyte proliferation via H2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Mast Cell-Dependent Down-Regulation of Antigen-Specific Immune Responses by Mosquito Bites

“…Histamine, whose mast cells are the major storage site, is an attractive candidate as a dendritic cell modulator especially during early phases of the immune response. Histamine was reported to have immunosuppressive effects, such as inhibition of polymorphonuclear chemotaxis (23) and monocyte IL-12 secretion (24), as well as induction of IL-10 production (25). Interestingly, analysis of cytokine production by cultured LN cells after completion of DTH response indicate that increased production of IL-10 by mosquito bites was correlated with the presence of mast cells.…”

Transfusion-transmissible infections and transfusion-related immunomodulation

“…These mediators are contained in intracellular WBC granules, and are released in a time-dependent manner as the WBCs deteriorate during storage [59]. It has been shown that at least some of these biologic response modifiers (histamine, eosinophil cationic protein, eosinophil protein X, TGF-β) may contribute to the development of immunosuppression and tissue damage by inhibition of neutrophils, cytotoxic T-cells and natural killer cells [60], [61], [62], [63].…”

Forskolin-inducible cAMP Pathway Negatively Regulates T-cell Proliferation by Uncoupling the Interleukin-2 Receptor Complex

“…reports have extensively documented the inhibitory effects of adenylate cyclase linked G protein-coupled receptor agonists on lymphocyte proliferation (16,19,21,35). To identify the molecular mechanism responsible for this effect, we first sought to determine whether Fsk, a potent adenylate cyclase activator, affects the proliferation of the human T-cell lines such as Kit 225 ( was due to an increase in cAMPi, cAMPi generation was measured using an ELISA.…”