Lappin, D. and Whaley, K. (1980) Effects of histamine on monocyte complement production. I. Inhibition of C2 production mediated by its action on H2 receptors. Clinical and Experimental Immunology, 41(3), pp. 497-504.
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Abstract
Histamine produced dose-dependent inhibition of the production of the second complement component (C2) by monocytes in tissue culture. The effect was not associated with either cell death, as ascertained by trypan blue exclusion, or loss of cells from the monolayer, as determined by measuring their DNA content. The specificity of the response was shown by the failure of histidine or histamine metabolites to inhibit C2 production. Preincubation of histamine with histaminase also abrogated the histamine effect. The kinetics of the effect were extremely rapid and irreversible, most of the reduction being achieved during a 5-min exposure to histamine. The H2 receptor antagonist cimetidine was able to prevent the histamine response, whereas chlorpheniramine, the H1 receptor antagonist, had no effect. Dimaprit and 4-methyl histamine, H2 receptor agonists, simulated the effect of histamine whereas the H1 receptor agonist 2-(2-aminoethylthiazole) was ineffective, confirming that the effect of histamine on C2 production by monocytes is mediated by the H2 receptors. Thus histamine, released from basophils or mast cells by the C3 and C5 cleavage products C3a and C5a respectively, may exert a negative feedback on further C3 and C5 cleavage by limiting the formation of the C3 (C42) and C5 (C423b) convertases.
| Item Type: | Articles |
|---|---|
| Status: | Published |
| Refereed: | Yes |
| Glasgow Author(s) Enlighten ID: | Lappin, Dr David |
| Authors: | Lappin, D., and Whaley, K. |
| Subjects: | Q Science > QR Microbiology > QR180 Immunology |
| College/School: | College of Medical Veterinary and Life Sciences > School of Medicine, Dentistry & Nursing > Dental School |
| Journal Name: | Clinical and Experimental Immunology |
| Publisher: | Wiley-Blackwell Publishing Ltd. |
| ISSN: | 0009-9104 |
| ISSN (Online): | 1365-2249 |
| Related URLs: |
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