Neutrophil migration in mice induced by a mannose-binding lectin isolated from Annona coriacea seeds
A novel 14-kDa lectin from Annona coriacea seeds (ACLEC) with hemagglutinating activity on erythrocytes has been recently described. Since plant lectins are known to present inflammatory activity, this study aimed to investigate the leukocyte migration induced by ACLEC, and inflammatory mediators in...
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Veröffentlicht in: | Toxicon (Oxford) 2006-10, Vol.48 (5), p.529-535 |
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Zusammenfassung: | A novel 14-kDa lectin from
Annona coriacea seeds (ACLEC) with hemagglutinating activity on erythrocytes has been recently described. Since plant lectins are known to present inflammatory activity, this study aimed to investigate the leukocyte migration induced by ACLEC, and inflammatory mediators involved in this phenomenon. Male Swiss mice were intraperitoneally injected with ACLEC (3–100
μg/cavity), and at 4–96
h thereafter the leukocyte counts in peritoneal lavage fluid were evaluated. ACLEC induced a dose-dependent neutrophil accumulation, reaching maximal responses at 16
h after injection (approximately 40-fold increase for 30
μg/cavity). Significant accumulation of mononuclear cells was observed at 72
h (2.7-fold increase). The carbohydrate mannose nearly abolished the neutrophil influx, whereas sucrose, glucose and galactose had no effect. Dexamethasone, the cyclooxygenase-2 (COX-2) inhibitor celecoxib and the Platelet activating factor (PAF) receptor antagonist PCA4248 significantly reduced ACLEC-induced neutrophil influx. The tachykinin NK
1 antagonist SR140333, the tachykinin NK
2 antagonist SR48968, the non-selective NO inhibitor L-NAME, the selective inducible NOS inhibitor aminoguanidine and the lypoxygenase inhibitor AA861 all failed to modify the ACLEC-induced responses. In conclusion, ACLEC is able to attract neutrophils into the mice peritoneal cavity by mechanisms involving interactions of the lectin with cell-specific mannose recognition, leading to the release of COX-2-derived mediators and PAF. |
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ISSN: | 0041-0101 1879-3150 |
DOI: | 10.1016/j.toxicon.2006.07.001 |