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Human monocytes exposed to particles reacting with receptors of one specific type demonstrate a markedly reduced phagocytosis of particles reacting with receptors of another type. The phagocytosis of yeast particles (Saccharomyces cerevisiae) coated with C3 fragments and of uncoated ones by monocytes can inhibit the subsequent endocytosis of sheep erythrocytes sensitized with IgG antibody and vice versa. The erythrocytes were labelled with 51Cr and the yeast particles with 125I. The dependence of the receptor-ligand reaction on temperature and time of preincubation, as well as on ratio of cell and particle, suggests that this cross-inhibition may be associated with plasma membrane modulations beginning with the attachment of ligands to a receptor and followed by their endocytosis. The differences between the functions of temperature, time, and concentration in inhibition caused by different receptor-ligand reactions suggest that these membrane modulations are probably ligand-specific processes.

We have observed the symptoms of systemic inflammatory response syndrome (SIRS) in male rats intoxicated by carbon tetrachloride (CCl4). Severe hypothermia, tachypnoea and increase in the heart beat min were diagnosed. These symptoms developed in the first hour of intoxication. The hepatic dysfunction was characterized by elevated bilirubin levels. In the sera we have measured increases in the activity of secretable (group II) phospholipase A2 sPLA2 (2,8x) and 6-ketoprostaglandin F1α (KPGF) (1,44x). Supposedly the free radicals derived from CCl4—mainly trichloromethyl—could induce the prompt reaction of SIRS and the release of sPLA2 as well as the formation of KPGF. Our findings show that in the early phase of CCl4 intoxication the symptoms of SIRS can be related to elevation of sPLA2 and the products of cyclooxygenase II.

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