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Abstract

KM+, a lectin purified from Artocarpusintegrifolia seeds, is an attractant for neutrophils, and has properties similar to fMLP, IL-8 and MNCF. The endogenous lectin MNCF, inhibits carrageenan-induced neutrophil migration when intravenously administered in rats. In an attempt to mimic the activity of MNCF with KM+, we determined the effect of intravenous (iv) injection of KM+ (5 microg) on neutrophil migration to the peritoneal cavity of Wistar rats induced by KM+ (50 microg, intraperitoneal, ip), fMLP (5 ng, ip) and carrageenan (300 microg, ip). Initially we evaluated the effect of the time interval between intravenous and intraperitoneal administration of KM+. The intervals ranged from 20 to 120 min and progressively stronger inhibition was observed with increasing time intervals up to a maximum of 60 min, with effect decreasing thereafter. With injections at the optimum interval of 60 min, we observed that KM+ inhibited KM+- and carrageenan-induced neutrophil migration by 72%, and fMLP-induced migration by 56%. White cell counts for Wistar rats that only received KM+iv, performed at 0 to 120 min intervals after injection, revealed early neutropenia lasting 60 min, followed by a marked increase in circulating neutrophils that reached a maximum of twice the initial levels within 90 min and after 120 min returned to levels near to that observed before intravenous administration of KM+. These results indicate that when KM+ is present in the intravascular space, it produces an inhibitory effect on neutrophil migration similar to that caused by the intravenous administration of other chemoattractants, regardless of whether they act through a mechanism independent of carbohydrate recognition, as does IL-8, or are dependent on carbohydrate recognition, like MNCF.

Mast Cell Degranulation Induced by Lectins: Effect on Neutrophil Recruitment

“…In this study, the mammalian lectin MNCF and the plant lectin KM+, both known to be neutrophil attractants [6, 26], were shown to induce mast cell degranulation. Mast cell activation induced by MNCF or KM+ was shown to provide an amplification loop for the neutrophil recruitment promoted by these lectins.…”

“…Lectins are ubiquitously distributed in the nature and their binding to cell surface glycans can induce cell activation that then leads to specific cellular responses. Macrophage-derived neutrophil chemotactic factor (MNCF), a D- galactose-binding animal lectin, [2, 3], produced by activated macrophages [2, 3]and KM+ a D -mannose-binding plant lectin, extracted from the seeds of Artocarpus integrifolia [4]are known to be neutrophil migration inducers [5, 6]. …”

Characterization and optimization of ArtinM lectin expression in Escherichia coli

“…As a consequence, ArtinM administration to mice has been shown to confer resistance to Leishmania [6,8], and Paracoccidioides brasiliensis [7] infections. The lectin ArtinM is also capable of inducing neutrophil haptotactic migration mediated by the simultaneous interaction of its carbohydrate recognition domains (CRDs) with cell surface N-glycans (linked to the CXCR2 molecule) [9] and extracellular matrix N-glycans (linked to laminin) [10-12]. An amplification loop for the in vivo ArtinM inflammatory activity is provided by mast cell degranulation, which is most likely due to the lectin interaction with glycans on FcRI [13].…”