Sephadex induces eosinophil migration to the rat and mouse peritoneal cavity: involvement of mast cells, LTB4, TNF-alpha, IL-8 and PAF.
OBJECTIVE
In this study we investigated the chemotactic mediators involved in the Sephadex-induced eosinophil migration into the peritoneal cavities of rats and mice, and which resident peritoneal cells release these mediators.


METHODS
Sephadex suspension was injected into the peritoneal cavities of rats or mice which were pretreated, or not, with specific drugs that inhibit synthesis or production of the inflammatory mediators and eosinophil chemotactic activities were observed. To investigate the role of resident peritoneal cells as a source of these chemotactic factors, the macrophage population was enhanced or the mast cell population was depleted. The resident cells were also stimulated, in vitro, with Sephadex and the chemotactic activity of the supernatants was determined.


RESULTS
Sephadex induced dose and time dependent eosinophil migration in rats and mouse, which were inhibited by dexamethasone and MK 886. BN 52021 only affected the eosinophil migration into the mouse peritoneal cavity. An increase in the macrophage population did not alter the eosinophil migration induced by Sephadex in rat or mouse. However, mast cell population depletion reduced eosinophil migration in rats, but did not alter the migration in mice. Sephadex-stimulated rat mast cells released an eosinophil chemotactic factor whose release was inhibited by dexamethasone and MK 886. Anti-TNF-alpha and anti-IL-8 Abs inhibited the chemotactic activity of the mast cell supernatant.


CONCLUSIONS
Sephadex-induced eosinophil migration into the rat peritoneal cavity is dependent on mast cells, which release LTB4, TNF-alpha and CINC-1. Conversely, Sephadex-induced eosinophil migration into the mouse peritoneal cavity is mediated by PAF and LTB4, which are not released from resident macrophages or mast cells.
Oliveira
S H P
SH
Department of Pharmacology, Faculty of Medicine of Ribeirão Preto, University of Sao Paulo, Brazil. shpoliv@hotmail.com
Costa
C H S
CH
Ferreira
S H
SH
Cunha
F Q
FQ
D000818:Animals; D002465:Cell Movement / Q000187:drug effects; D054360:Chemokine CXCL1; D018925:Chemokines / Q000502:physiology; D019743:Chemokines, CXC; D002630:Chemotactic Factors / Q000502:physiology; D003911:Dextrans / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004804:Eosinophils / Q000187:drug effects* / Q000502:physiology; D036341:Intercellular Signaling Peptides and Proteins / Q000502:physiology; D016209:Interleukin-8 / Q000502:physiology*; D007975:Leukotriene B4 / Q000502:physiology*; D008297:Male; D008407:Mast Cells / Q000502:physiology*; D051379:Mice; D010529:Peritoneal Cavity / Q000166:cytology*; D010972:Platelet Activating Factor / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D054360:Chemokine CXCL1; D018925:Chemokines; D019743:Chemokines, CXC; D002630:Chemotactic Factors; C475895:Cxcl1 protein, mouse; C513297:Cxcl1 protein, rat; D003911:Dextrans; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8; D010972:Platelet Activating Factor; D014409:Tumor Necrosis Factor-alpha; D007975:Leukotriene B4; C025614:sephadex