Histamine binding to H2 receptors stimulates phospholipid methylation in mast cells

Abstract

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...

Histamine Acting on H2 Receptors Stimulates Phospholipid Methylation in Synaptic Membranes of Rat Brain

“…The present data show that histamine stimulates PE methylation in rat brain synaptosomes, just as Tolone et al ( 1982) have previously shown in mast cells. Histamine ( 10 p M ) caused a rapid increase and decrease in phospholipid methylation in rat brain synaptosomes, with the peak in [3H]methyl incorporation being achieved at 45 s (Fig.…”

Histamine H2receptor signaling × environment interactions determine susceptibility to experimental allergic encephalomyelitis

“…H 2 R couples to second messenger signaling pathways via the stimulatory G protein, Gα s (10), leading primarily to activation of adenylate cyclase and increased cAMP (11–18). In addition, the activation of H 2 R leads to phospholipid methylation (19), an increase in the slow inward Ca 2+ current (20), stimulation of phospholipase C, intracellular Ca 2+ mobilization (21, 22), and inhibition of phospholipase A 2 activation (23). Furthermore, histamine binding to H 2 R leads to the activation of c‐Fos (8, 24, 25), c‐Jun (20), protein kinase C, and p70S6kinase (26).…”

Histamine Increases Phospholipid Methylation and H2‐Receptor‐Adenylate Cyclase Coupling in Rat Brain

“…have proposed that N-methylation of membrane phospholipids plays an important role in the transduction of biochemical signals through membranes. Thus, PMTases in various tissues have been activated by such agents as dopamine in rat brain neurons (Leprohon et al, 1983), isoproterenol in rat reticulocyte ghosts (Hirata et al, 1979a), histamine in mast cells (Tolone et al, 1982), thyrotropin-releasing hormone in rat pituitary glands (Prasad et al, 1985), lectins in lymphocytes or mast cells (Hirata et al, 1979b), immunoglobulins in mast cells (Ishizaka et al,198 l), angiotensin or vasopressin in hepatocytes (Alemany et al,198 I), and glucagon in hepatocytes (Castano et al, 1980). Moreover, recent work in our laboratory has shown that histamine stimulates phospholipid methylation in synaptic membranes of rat brain acting on H2-receptors (Ozawa et al, 1987).…”