Effect of Drugs on the Increase in Cell Numbers in the Peritoneal Cavity of the Actively Sensitised Mouse after Intraperitoneal Challenge with Antigen

Abstract

The injection of antigen into the peritoneal cavity of actively sensitised mice produced an increase in the number of neutrophils in peritoneal washings collected 4 h later but after 1 day the numbers had returned to control levels. The increase in numbers of mononuclear cells and eosinophils in the peritoneal washings peaked at 2 days and persisted for at least 5 days. Dosing the mice with phenidone, a dual inhibitor of the cyclo-oxygenase and lipoxygenase pathways of arachidonic acid metabolism, potentiated the neutrophil infiltration at 4 h but had no significant effect upon the subsequent mononuclear cell and eosinophil infiltration. In contrast, treatment with the corticosteroid, dexamethasone, reduced the infiltration by all three types of cells, providing further evidence that the corticosteroids can inhibit immune-induced cellular infiltrations by mechanisms other than the inhibition of arachidonic acid metabolism. Isoprenaline, given to the mice before antigen challenge, had no effect on the subsequent neutrophil infiltration, but repeated doses did inhibit the mononuclear cell and eosinophil infiltration measured 4 days later. Aminophylline, disodium cromoglycate and cyproheptadine had no effect upon the cellular changes.

Direct In Vivo Monitoring of Acute Allergic Reactions in Human Conjunctiva

“…As suggested in animal (33)(34)(35) and human studies, allergen challenge induces strong leukocyte recruitment, as has been detected in tissue biopsies, (36 -38) although histamine alone cannot induce any extravasation (30,36,39). Previous results are in line with our data that histamine is sufficient to induce leukocyte rolling, but endogenous mediators other than histamine are likely to participate in the reduction in velocity of the rolling leukocytes and in the actual extravasation during the generation of acute allergen-induced inflammation (7).…”

Tumour necrosis factor‐alpha and leukotriene B4 mediate the neutrophil migration in immune inflammation

“…OVA challenge induced a dose‐ and time‐dependent neutrophil migration in immunized mice, which peaked 4 h after challenge and returned to basal levels after 24 h, when a significant eosinophil and mononuclear cell infiltrate was observed. Similar kinetics for cell infiltration induced by antigen challenge in immunized mice and other species have been described (Abe et al ., 1994; Klein et al ., 1995; Metzger et al ., 1996; Sharpe & Smith, 1979; Spicer et al ., 1985; 1986; Zuany‐Amorim et al ., 1993). We found that OVA‐induced neutrophil accumulation was dependent on endogenous release of LTB 4 and cytokines, since neutrophil recruitment was inhibited by MK 886, an LTB 4 synthesis inhibitor (five‐lipoxygenase activating protein (FLAP) inhibitor; Miller et al ., 1990), by CP 105,696, an LTB 4 receptor antagonist (Koch et al ., 1994), and by dexamethasone, a glucocorticoid that inhibits eicosanoid and cytokine production.…”

Inhibition of PAF-induced eosinophil accumulation in pulmonary airways of guinea pigs by anti-asthma drugs.

“…Studies in the rat (19), guinea pig (6) and mouse (20) indicate that drugs such as ketotifen or cromoglycate may achieve inhibition irrespective of the stimulus used to induce eosinophil accumu lation. There are few clinical reports on the effect of anti-asthma drugs on eosinophils in asthma.…”