Seasonal variation in the function of blood monocytes obtained from healthy nonsmokers, asymptomatic smokers, and smokers with chronic bronchitis.

The present study focused on two questions: What effects do cigarette smoking and chronic bronchitis have on the function of the precursors of alveolar macrophages, the blood monocytes? Can seasonal variations affect the function of these cells? Phagocytic activity (the proportion of yeast-ingesting cells and the mean number of yeast particles per ingesting cell) and metabolism of arachidonic acid [secretion of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) in zymosan-stimulated cultures] were studied as markers of monocyte function during three seasons: spring (May-June), autumn (November-December), and winter (February). Smokers with chronic bronchitis (SCBs) and asymptomatic smokers (ASs) had a lower proportion (p < 0.05) of ingesting monocytes than healthy nonsmokers (HNSs) during spring, but not during the other two seasons. The secretion of PGE2 was highest during autumn and lowest during spring in the monocytes of all three groups. In autumn, LTB4 secretion was increased in the monocytes of HNSs (p < 0.05) but not in those of ASs and SCBs. LTB4 secretion was similar in all groups during the other two seasons. Cigarette smoking and chronic bronchitis seem to impair the function of monocytes and may thereby affect the systemic host defense activity. Cells collected during autumn were generally more active than those sampled in spring, indicating marked seasonal variation in the function of monocytes from all three groups.

High dose aerosol pentamidine for secondary Pneumocystis carinii pneumonia prophylaxis in AIDS patients.

In a prospective trial of aerosolized pentamidine as secondary prophylaxis for Pneumocystis carinii pneumonia (PCP) 18 patients received 400 mg once weekly for a mean period of 15.5 months. Pentamidine aerosol was administered with an MA2 jet nebulizer. No PCP relapses were observed and no serious side effects occurred.

Herpes simplex virus--the most frequently isolated pathogen in the lungs of patients with severe respiratory distress.

308 consecutive patients with severe or complicated respiratory tract infections underwent fiber-optic bronchoscopy in the search for a microbiological etiology. Protected brush specimens were used for bacterial cultures and bronchoalveolar lavage (BAL) for virus isolation and cytological examination. Herpes simplex virus (HSV) was the most commonly found pathogen and was isolated in 37 patients. 20 (54%) of them also had serological and/or cytological signs of HSV infection. 132 patients required assisted ventilation (AV) and in this group 34 (92%) of the 37 HSV positive patients were found. Isolation of HSV was significantly (p less than 0.001) associated with AV compared to patients not requiring AV. Of all patients treated with AV 26% had positive HSV isolation in conjunction with suspected acute lower respiratory infection. Coinfection with HSV and bacteria occurred in only 8 (22%) patients. HSV was more common in patients with burns (47%) compared to other patient groups such as patients with AIDS (3%) or other immunodeficiencies (9%).

Short course of aerosol pentamidine as treatment of Pneumocystis carinii pneumonia in AIDS.

Since July 1987, 20 HIV-positive patients with Pneumocystis carinii pneumonia (PCP) admitted to the Department of Infectious Diseases, Malmö General Hospital, Sweden have been treated with 10 consecutive days of aerosol pentamidine as sole antimicrobial therapy in a prospective open non-controlled trial. 16 patients (80%) responded to 10 days of 400 mg aerosol pentamidine daily. One patient responded after a prolonged treatment, one patient received simultaneous trimethoprim-sulfamethoxazole due to lack of improvement during aerosol therapy. Two patients died 26 and 41 days after initiation of treatment. No systemic side effects occurred. In conclusion, we found that 10 days of aerosol pentamidine may be a safe and effective treatment of PCP. Controlled studies are needed.

Seasonal variation in the phagocytic activity and arachidonic-acid metabolism of human blood monocytes in healthy non-smokers, smokers and chronic bronchitics.

Peripheral blood monocytes are precursor cells to alveolar macrophages (AMs). Many studies have been performed with a view to assessing the differences, in respect of morphology and function, between the AMs of smokers and those of non-smokers. Disturbed host-defence activity of smokers' AMs is reflected by, for instance, decreased phagocytic activity and impaired arachidonic acid metabolism. However, very little attention has been paid to the question what effects cigarette smoking and chronic bronchitis may have on the function of the precursors of these cells--the blood monocytes. The collection of blood monocytes is much less laborious than the sampling of AMs. Therefore, it would be a great advance if the deteriorated host defence in chronic bronchitis could be detected and followed by studies of blood monocytes. However, a seasonal variation in monocyte function, discussed in this paper, may counteract the advantage inherent in repeated sampling. This seasonal variation in cellular host-defence mechanisms should be taken into account when designing longitudinal intervention trials in chronic bronchitis.

Studies on the role of antileukoprotease in respiratory tract diseases.

Antileukoprotease, an inhibitor of granulocyte elastase, was studied in paired sera from 19 patients with pneumonia and from 9 patients with cholecystolithiasis. The circulating level of antileukoprotease was significantly higher in patients with pneumonia compared with patients with cholecystolithiasis. In the latter group, surgery raised the level of general acute phase reactants, but did not affect the level of antileukoprotease. In sera from patients with pneumonia, antileukoprotease was recovered in a free and active form, as shown by gel-filtration of sera before and after the addition of leukocyte elastase. A local protective function of antileukoprotease is suggested by the finding that antileukoprotease was bound to granulocyte elastase in purulent bronchial secretions.