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Updated: Jul 5, 2026

Detecting Migration and Infiltration of Neutrophils in Mice
Published on: February 6, 2020
Mechanism of calcium hydroxide-induced neutrophil migration into air-pouch cavity
Mariana Machado Teixeira de Moraes Costa1, Sandra Helena Penha de Oliveira, João Eduardo Gomes-Filho
1Department of Pediatric Dentistry, School of Dentistry, Sao Paulo State University, Araçatuba, Brazil. moraes_mari@hotmail.com <moraes_mari@hotmail.com>
Abstract:
The aim of this study was to investigate cellular migration induced by calcium hydroxide to air-pouch cavities in mice. The migration was more specific to neutrophil and was dose and time dependent (peaking 96 h after stimulation). This migration was inhibited by pretreatment with thalidomide, indomethacin, MK886, meloxicam, dexamethasone, MK886 associated with indomethacin, and MK886 associated with indomethacin and dexamethasone. The air-pouch exudate from animals stimulated with calcium hydroxide showed an increase of leukotriene-B(4) (LTB(4)), interleukin-1beta, tumor necrosis factor alpha (TNF-alpha), cytokine-induced neutrophil chemoattractant (KC), and macrophage inflammatory protein 2 (MIP-2) release. Pretreatment with 3% thioglycollate increased the macrophage population in the air pouch but did not change neutrophil migration. Depleting the resident mast cells through chronic pretreatment with compound 48/80 did not alter neutrophil migration in response to calcium hydroxide. It was possible to conclude that calcium hydroxide-induced neutrophil migration to the air-pouch cavity in mice is mediated by LTB(4), TNF-alpha, KC, MIP-2, and prostaglandins, but it was not dependent on macrophages or mast cells.
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