Role of Resident Peritoneal Cells in Eosinophil Migration Induced by Saline

Abstract

In the present study, we investigated the role of resident peritoneal cells as well as the mediators involved in the eosinophil migration induced by large volumes of physiological saline. Two consecutive intraperitoneal injections of saline given 48 h apart, induced a selective recruitment of eosinophils into the cavity. This response was not observed with phosphate-buffered saline (PBS). Saline-induced eosinophil migration may be mediated at least in part by LTB₄, since the lipoxygenase inhibitors BW A4C and MK 886 prevented the response. In the presence of saline, but not of PBS, mast cells and macrophages incubated in vitro released a factor which induced eosinophil migration when injected into the peritoneal cavity of rats. This release was inhibited by BW A4C and MK 886. These results indicate the importance of mast cells and macrophages in the eosinophil migration induced by saline and suggest the participation of LTB₄ in this phenomenon. An abrupt reduction in the extracellular potassium concentration at the membrane of resident cells may be responsible for the saline effects since addition of potassium ions to saline abolished the eosinophil chemotactic activity of the same as well as its ability to stimulate the release of eosinophil chemotactic factor in vitro. Dexamethasone blocked both the saline-induced eosinophil migration and the release of eosinophil chemotactic factor by mast cells and macrophages. Pretreatment of the animals with dexamethasone inhibited the eosinophil migration induced either by the supernatants of saline-stimulated mast cells and macrophages or by LTB₄. These results indicate that the release of additional mediators is necessary in order to account for the final eosinophil migration. This conclusion is supported by the observation that peritoneal cavities depleted of resident cells did not demonstrate eosinophil migration when challenged with either LTB₄ or the supernatants of saline-treated cells.

Eosinophilia is attenuated in experimental colitis induced in IL-5 deficient mice

“…The numbers of eosinophils are much higher if the colitis is induced by a lower concentration of DSS although the significance of this finding is unclear. Macrophages and their products are important factors in the recruitment of eosinophils 14,15 but we did not demonstrate any difference in numbers of macrophages in the inflammatory infiltrate between IL-5 deficient mice and controls. Our results, however indicate that the recruitment of eosinophils to the inflamed region is influenced by the activity of IL-5 but that the reduced eosinophil responses in IL-5 deficient mice did not alter the severity of the disease or the extent of tissue damage.…”

Participation of lnterleukin-5 and lnterleukin-8 in the Eosinophil Migration Induced by a Large Volume of Saline

“…4). The super natants of mast cells and macrophages incubated with saline also induced eosinophil migration 6 h after the intraperito neal injection, and this lasted for 24 h [29].…”

“…This response was not observ ed with phosphate-buffered saline (PBS). The mechanism by which saline induces eosinophil migration may involve an alteration of cell membrane properties resulting from a lowering of the potassium ion concentration in the extracel lular environment [29]. Recently, we demonstrated that this migration is mediated by LTB., released by the resident mast cells and macrophages [29].…”

“…The mechanism by which saline induces eosinophil migration may involve an alteration of cell membrane properties resulting from a lowering of the potassium ion concentration in the extracel lular environment [29]. Recently, we demonstrated that this migration is mediated by LTB., released by the resident mast cells and macrophages [29]. In the present study, we have shown that mast cells and macrophages incubated with saline also release IL-5 and IL-8, both of which are involved The supernatants were pretreated with PBS ( ), control serum (C'S) or with IL-I.…”

“…Leuko triene SJ is probably the lipoxygenase metabolite involved in the process since there are data showing that this mediator is chemotactic for eosinophils [46]. Interestingly, the eosi nophil chemotactic activity o f LTB4 is also dependent on the presence of resident mast cells and macrophages [29], This fact, together with the observation that the inhibition of one o f these mediators (IL-5, IL-8 or LTB4) completely blocked the eosinophil migration induced by the superna tants of mast cells and macrophages stimulated with saline suggest that they act synergistically.…”