Leukocytes histamine

Mata E, Gueant JL. Moneret-Vautrin DA, Bermejo N, Gerard P, Nicolas JP. Laxenaire MC Chnical evaluation of in vitro leukocyte histamine release in allergy to muscle relaxant drugs. Allergy 1992 47 471. 

Scinto J, Enrione M, Bernstein D, Bernstein IL. In vitro leukocyte histamine release to progesterone and pregna-nediol in a patient with recurrent anaphylaxis associated with exogenous administration of progesterone. J Allergy Clin Immunol 1990 85 228. 

Additional biological tests have been suggested to improve the accuracy further. The leukocyte histamine release test has been found helpful (75) but it is expensive and time-consuming. Several surface molecules have been studied as markers, for example CD63. IgE-mediated degranulation of basophils after incubation of the patient s serum with a neuromuscular blocking agent can... 

BW 437C, a new oral carboxythioxanthone-10,10-dioxide, is reported to be a more effective inhibitor of human leukocyte histamine release than DSCC or doxantrazole f301. 

Inflammation. Figure 1 Sequence of events in the recruitment of leukocytes in postcapillary venules adjacent to injured tissue. At the site of lesion, diverse reactive substances stimulate the endothelium to produce inflammatory cytokines, chemoattractants and other inflammatory mediators. The cytokine-activated endothelium expresses adhesion molecules that lead to the low affinity interactions between leukocytes and endothelium, which is mediated by selectins and described as rolling. Subsequently integrins mediate the firm adhesion of leukocytes, which allows emigration of the cells from venules into the interstitial compartment. Activated mast cells, PMNs and macrophages secrete cytokines (TNFa), lipid mediators (LTB4) and other inflammatory players (histamine, NO). 

S Molecular cloning and characterization of a novel 62 type of histamine receptor preferentially expressed in leukocytes. J Biol Chem 2000 275 36781. 

Oda, T., Morikawa, N., Saito,Y., Masuho,Y. and Matsumoto, S. Molecular cloning and characterization of novel type of histamine receptor preferentially expressed in leukocytes. /. Biol. Chem. 275 36781-36786, 2000. 

Acid acetone extracts of human and rodent leukocytes (RBL-cells) have been found to contain immunoreactive SOM (iSOM) and immunoreactive SP (iSP) as determined by radioimmunoassay [144], Quantities of the peptides varied from 325 pg iSOM/107 cells for human monocytes and 272 pg iSOM/107 cells for RBL-cells to 4.4 pg iSOM/107 cells for human T cells. iSP was highest in murine bone marrow-derived mast cells (64 pg iSP/107 cells) and RBL-cells (23 pg iSP/107 cells) and lowest in human T and B lymphocytes (2.5 and 1.2 pg iSP/107 cells, respectively). Interestingly, the murine bone marrow-derived mast cells had the highest ratio of iSP to iSOM. Preliminary chromatographic results show a large and a small SOM (SOM-28 and SOM-14, respectively). SOM-14 (3 x 10 9 M) has been shown to inhibit histamine release and LTC4 generation from murine bone marrow-derived mast cells stimulated by anti-IgE serum [144]. 

On the neutrophil, the major selectin expressed is L-selectin. This molecule is constitutively expressed on mature neutrophils but may be expressed at low levels (50% of adult) in neonates. Stimulation of endothelial cells with thrombin, histamine, IL-1 and some other agents induces neutrophils (and other leukocytes) to leave the circulation and adhere to the endothelium. They do this by rolling onto the surface of the endothelium, to which they attach via P-selectin translocated from storage sites in Weibel-Palade bodies to the surface of the endothelium upon activation. The expression of P-selectin is short-lived and is replaced on the endothelial surface by E-selectin (whose expression is also regulated by some cytokines), which continues the endothelial-leukocyte interaction. 

Kubes P. Kanwar S Histamine induces leukocyte rolling in post-capillary venules. A P-selectin-mediated event. J Immunol 1994 152 3570-3577. 

Yamaki K, Thorlacius H. Xie X. Lindbom L, Hedqvist P. Raud J Characteristics of histamine-induced leukocyte rolling in the undisturbed microcirculation of the rat mesentery. Br J Pharmacol 1998 123 390-399. 

Pierkes M, Bellinghausen I, Hultsch T, Metz G, Knop J, Saloga J Decreased release of histamine and sulfi-doleukotrienes by human peripheral blood leukocytes after wasp venom immunotherapy is partially due to induction of IL-10 and IFN- production of T cells. J Allergy Clin Immunol 1999 103 326-332. 

Small airway constriction and recruitment of leukocytes on pulmonary surfaces are prominent, documented responses to the inhalation of cotton dust. Currently, one or both of these effects are generally ascribed to endotoxin (8-10), to antigen-antibody reactions (11), to lacinilene C-7 methyl ether (1, 13), to a low molecular weight ( 1000 daltons), neutral, highly water soluble substance that is stable in boiling water and found in cotton bracts (14), to chemotaxins present in cotton mill dust extracts (15, 16) or to histamine releasing substances (17). 

Mechanisms of Complement Activation. Complement is a major mediator of the inflammatory response. Complement recruits and enlists the participation of humoral and cellular effector systems, induces histamine release from mast cells and directs migration of leukocytes (chemotaxis), in addition to producing phagocytosis and the release of lysosomal constituents from phagocytes. 

Potential etiologic agents in cotton dust that release histamine are shown in Table VII. Some of these are effector molecules having potent biological effects in minute concentrations, i.e. peptides, which may act directly to affect chemotaxis and leukocyte recruitment, and also to release histamine and stimulate respiratory smooth muscle contraction. These bifunctional effector molecules are of major importance in considering pathogenic mechanisms in byssinosis. 

Some agents are bifunctional, causing the release of histamine and recruiting leukocytes. Bifunctional mediators include bacterial peptides, endotoxins, DNA, C3a, C5a and bradykinin. Each of these substances can exert dual effects. This may either occur directly, as in the case of bacterial peptides and bradykinin causing chemotaxis and bronchial smooth muscle contraction, or indirectly, as endotoxin and DNA conversion of complement. C3a and C5a act indirectly as complement fragments to effect histamine release, which in turn contracts bronchial smooth muscle. However, both appear to act directly to effect chemotaxis with C5a, the more potent fragment. 

---