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Peripheral blood neutrophils were harvested and exposed acutely in vitro to physiologically attainable levels of cigarette smoke. The adherence of radiolabeled neutrophils subsequently to alveolar epithelial cell monolayers was measured. In contrast to control cells, smoke-exposed neutrophils were significantly less adherent and failed to increase their adherence following stimulation with phorbol ester or f-met-leu-phe (fMLP). Flow cytometric analysis of the cell surface adhesion protein CD18 demonstrated no significant change in expression following in vitro smoke exposure and, furthermore, no increase in surface CD18 of smoke-exposed cells following consecutive fMLP stimulation was demonstrated. Acute in vivo cigarette smoking of up to 4 cigarettes also did not alter peripheral blood neutrophil CD18 expression. Cell spreading and chemokinesis, but not chemotaxis, was also impaired following in vitro smoke exposure. These data suggest that acute cigarette smoke may impair the crucial neutrophil functions of adherence and movement. However, the chronic effects of cigarette smoke exposure may clearly differ.

SUMMARY The serum concentrations of the complement inactivators C1INH, C3bINA and 31H have been determined in patients with ulcerative colitis and Crohn's disease and their correlation with C3 and properdin factor B examined. The incidence of immunoconglutinins (IK) in these patients was investigated. Raised serum concentrations of CTINH and C3bINA have been found in patients with active disease, but no significant alteration was found in serum concentration of 31H. An increasing incidence of positive 1K titres was found with increased length of disease history. These results suggest continuing complement activation in these diseases.

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SUMMARY The inhibitory effects ofhydroxychloroquine on leucocyte motility have been compared with those ofprednisolone. It has been shown to have similar potency to prednisolone as an inhibitor of human neutrophil and monocyte motility. Hydroxychloroquine has then been compared with placebo in the prevention of an immune-complex experimental colitis in rabbits. Rectal biopsies were taken from rabbits 24 hours after initiation of colitis, coded, and graded histologically. The summated gradings for acute inflammation and goblet cell depletion had worsened more in the control rabbits (mean grade + 6.7) than in the treated rabbits (mean grade + 1.8) P<0.05. There was no difference in the mononuclear cell infiltrate between the two groups. Hydroxychloroquine, which is a potent inhibitor ofleucocyte motility, effectively prevents the acute inflammatory infiltrate in this experimental colitis model and therefore merits trial in human ulcerative colitis.Prednisolone and other glucocorticoids are effective treatment for ulcerative colitis. 1 2 One of the known effects of prednisolone is the inhibition of leucocyte chemotaxis,34 and this may be important for its therapeutic action. The 4-amino quinoline, chloroquine, has also been shown to inhibit chemotaxis of leucocytes3 as has its derivative hydroxychloroquine,5 although the latter has not previously been tested using human leucocytes. Chloroquine has also been shown to prevent the accumulation of neutrophils into experimental Arthus lesions.