Mediation of inflammatory ascites formation induced by macromolecules in mice.

Mediation of inflammatory ascites formation induced by macromolecules in mice. Acta Microbiol Immunol Hung. 2018 Feb 23;:1-12 Authors: Baintner K Abstract The first 60-min phase of inflammatory ascites formation was studied by intraperitoneally (i.p.) administered macromolecular inducers: yeast cell wall zymosan binds to specific macrophage receptors, polyethyleneimine (PEI) and concanavalin A (ConA), produces non-covalent cross-links on the surface of various cells, while λ-carrageenan may function as a contact activator. Depletion of peritoneal macrophages was performed by overnight pretreatment with diphtheria toxin in transgenic mice, resulting in a significant (p < 0.01) decrease in the induced formation of ascitic fluid. It was shown that induced ascites is mediated partly (PEI, ConA, and carrageenan) or completely (zymosan) by peritoneal macrophages. Inhibition of prostanoid synthesis with indomethacine or of the kallikrein/bradykinin system with aprotinin also produced a significant (p < 0.01) but incomplete inhibition. A slight additivity occurred between the different inhibitory effects. In another series of experiments, the i.p. administration of bradykinin (without a macromolecular inducer) also produced marked ascites, which was not affected by macrophage depletion. The origin of the macrophage-independent part of the induced ascites is best explained by the deformation of the mesothelial cell surface, res...
Source: Acta Microbiologica et Immunologica Hungarica - Category: Microbiology Authors: Tags: Acta Microbiol Immunol Hung Source Type: research