Human polymorphonuclear leukocytes were found to be able to synthetize and release substantial amounts of PGE2' when stimulated by a phagocytic stimulus such as zymosan particles coated with complement. Hydrocortisone, at a concentration of 10(-5) M, which proved to be effective in other biological systems, failed to inhibit phagocytosis and PG release.

The effects of adrenergic blocking agents on inflammation have been investigated in rats utilising passive cutaneous anaphylaxis induced with anti-BSA antibodies (rat IgGa or rabbit IgG) and BSA. It was concluded that blocking agents do not affect the pathways leading to the release of phlogistic mediators. Our findings have confirmed the role of catecholamines as factors controlling the inflammatory response and have suggested, furthermore, that hormonal activity is mediated by β-adrenergic receptors.

966 divided in the same manner into 3 groups of 6 animals each: infected, heat-exposed and control. All animals were then injected i.p. with 1 ml of a 10% suspension of washed sheep erythrocytes, while those of the infected group were additionally injected with a sublethal dose of live Salmonella enteritidis (0.0002 mg bacterial dry weight) s. 6 h later, the animals of the heat-exposed group were placed at an ambient temperature of 37 0C, while the thermodes of the hypothalamus-cooled group were perfused with water the temperature of which was regularly adjusted to induce a change in body temperature similar to that elicited by S. enteritidis s. Both experimental treatments, heat exposure and cooling of the hypothalamus, were discontinued after 5 days, and the animals were followed for another 11 days. Throughout the experiments, body temperature was measured every 8 h, and blood samples were taken at various time intervals. All methods, including the determination of the titre of antibodies against sheep erythrocytes, have been described in detail elsewhere 6. As there were no significant differences between the control animals with and without thermodes in any of the parameters studied in this work (see also Banet et al.6), these animals were pooled into a single control group. Furthermore, because 4 of the heat-exposed animals died during their exposure, though their rectal temperature never increased above 40 ~ the results of this group are not included in this report. 2 other animals, one each from the infected and hypothalamus-cooled groups, also died and their results were excluded. The cause of their death is not known, but it was noted that in both animals body temperature increased to nearly 41 ~ on the 3rd experimental day. Results. The figure summarizes the results. During the 1st 5 experimental days, the animals of the hypothalamus-cooled and infected groups maintained higher core temperatures (mean+ SE: 39.7+ 0.1 and 39.5 + 0.2 ~ respectively) than those of the control group (37.8+ 0.2 ~ p < 0.001, t-test). The animals of the hypothalamus-cooled group tended to have a lower titre of antibodies than those of the infected group but the highest titres achieved were not significantly different. The highest titres of both groups of experimental Experientia 38 (1982), Birkh~tuser Verlag, CH-4010 Basel/Switzerland animals were, however, significantly higher than those of the control ones (p < 0.005). Discussion. Intermittent cooling of the hypothalamus stimulates the humoral immune response 6. Since antibody titre increased after continuous and prolonged cooling of the hypothalamus, the present results show that the production of antibodies is not impaired when a high body temperature is sustained. Endogenous pyrogen has also been shown to increase the titre of antibodies 5, and this effect appears to be similar to that induced by intermittent cooling of the hypothalamus 6. Since cooling the hypothalamus simulates the febrile response 7, it is likely that the main effect of pyrogen on antibody titre is due...

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