Entamoeba histolytica in culture produces a pentapeptide (MQCNS). This oligopeptide inhibits the in vitro and in vivo locomotion of human monocytes, hence its denomination Monocyte Locomotion Inhibitory Factor (MLIF). The original isolated peptide and its synthetic construct display similar effects, among others, being inhibition of the respiratory burst in monocytes and neutrophils, decrease of Dinitrochlorobenzene (DNCB) skin hypersensitivity in guinea pigs and gerbils, and delay of mononuclear leukocytes in human Rebuck skin windows with inhibition of vascular cell Very late antigen (VLA)-4 and Vascular adhesion molecules (VCAM) in endothelia and monocytes. The MLIF molecular mechanism of action is unknown, but data reveal its implication in Nuclear factor-kappa B (NF-κB) and Mitogenactivated protein kinase (MAPK) pathways. This could explain MLIF multiplicity of biological effects. On the other hand, the amebic peptide has been useful in treating experimental amebiasis of the liver. The amebic peptide is effective in reducing inflammation induced by carragenin and arthritis in a Collagen-induced arthritis (CIA) model. Microarray data from experimental arthritis revealed an MLIF gene expression profile that includes genes that are involved in apoptosis, cell adhesion, extracellular matrix, and inflammation/chemotaxis. MLIF could be involved in unsuspected biological factions because there is increasing data on the peptide effect on several cell activities. This review also presents uses of MLIF as described in patents.
Keywords: Entamoeba histolytica, inflammation, peptide, protozoan Entamoeba, diarrhea, intestinal, E. histolytica, neutrophils, epithelioid cells, Polymorphonuclear, leukocytes, scarring, Monocyte locomotion inhibitory factor, trypsin, viruses, bacteria, fungi, skin lesions, microtubules, nitric oxide, Mononuclear phagocytes, anti-inflammatory, pharmacophore, MLIF PATENTS, pentapeptide, oligopeptide, leuko-cyte, amebiasis, Cystein, inflammatory accumulation, mRNA, endotoxins, phosphorylation, heterodimers, transcriptors, DNA, arthritis, genome, modeling, transduction pathways
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