The Cys-Asn-Ser carboxyl-terminal end group is the pharmacophore of the amebic anti-inflammatory monocyte locomotion inhibitory factor (MLIF)

Morales-Martínez, M. E.; Silva-García, Raúl; Soriano-Correa, Catalina; Giménez-Scherer, Juan Antonio; Rojas‐Dotor, Sara; Blanco-Favéla, Francisco; Rico-Rosillo, Guadalupe

doi:10.1016/j.molbiopara.2007.11.010

Cited by 13 publications

(11 citation statements)

References 7 publications

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“…Results showed that the Cys-Asn-Ser (C-N-S) tripeptide's carboxyl-terminal end group maintains biological and antiinflammatory properties, similar to full-length MLIF, whereas the initial Met-Gln-Cys (M-Q-C) and intermediate Gln-Cys-Asn (Q-C-N) peptides completely lose this effect. Thus, these results confirm that the last three amino acids are critical for MLIF function [27].…”

Section: Monocyte Locomotion Inhibitory Factorsupporting

confidence: 71%

Anti-inflammatory defense mechanisms of Entamoeba histolytica

Silva-García

Rico-Rosillo²

2010

Inflamm. Res.

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The monocyte locomotion inhibitory factor (MLIF), a heat-stable oligopeptide found in the supernatant fluid of Entamoeba histolytica axenic cultures, may contribute to the delayed inflammation observed in amoebic hepatic abscess. This factor was isolated by ultra-filtration and high powered liquid chromatography, obtaining a primary Met-Gln-Cys-Asn-Ser structure, identified afterwards as the carboxyl-terminal (…Cys-Asn-Ser) active site. The selective anti-inflammatory effects of the pentapeptide have been observed in both in vitro and in vivo models, using a synthetic pentapeptide to maintain the same anti-inflammatory conditions during the experimental assays. Anti-inflammatory effects observed include inhibition of human monocyte locomotion and the respiratory burst in monocytes and neutrophils, increasing expression of anti-inflammatory cytokines and inhibiting expression of the adhesion molecules VLA-4 and VCAM, among others. In this review, we will describe the effects of MLIF detected so far and how it might be used as a therapeutical agent against inflammatory diseases.

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Section: Monocyte Locomotion Inhibitory Factorsupporting

confidence: 71%

Anti-inflammatory defense mechanisms of Entamoeba histolytica

Silva-García

Rico-Rosillo²

2010

Inflamm. Res.

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“…Experimental studies have demonstrated that CNS possesses anti-inflammatory activity in vitro and in vivo, while CDS does not have in vitro anti-inflammatory activity [28,49]. Throughout the present discussion, we will consider the CNS tripeptide as the model peptide that possesses anti-inflammatory activity.…”

Section: Resultsmentioning

confidence: 99%

“…Therefore, quantum chemistry calculations are important to account for substituent effects that may provide insight into these electronic and physicochemical properties [6][7][8][11][12][13][14]26]. According to the latter, in earlier works our investigation group has studied the relationship between the physicochemical and structural properties of a small family of anti-inflammatory peptides [27][28][29]. Thus, the importance of the substituent effect of amino acid side chains on the physicochemical and chemical reactivity of these molecules was observed.…”

Section: Introductionmentioning

confidence: 99%

Importance of asparagine on the conformational stability and chemical reactivity of selected anti-inflammatory peptides

et al. 2015

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“…Moreover, ameba trophozoites interact with ␤2 integrins on the surface of neutrophils, induce their apoptosis through the phosphatidylinositol 3-kinase-mediated pathway (23), and activate intracellular signaling (19). Interestingly, the monocyte locomotion inhibitory factor is an anti-inflammatory oligopeptide produced by E. histolytica that inhibits locomotion of human monocytes (19).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₂Produced byEntamoeba histolyticaBinds to EP4 Receptors and Stimulates Interleukin-8 Production in Human Colonic Cells

Dey

Chadee

2008

Infect Immun

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Entamoeba histolytica pathogenesis in the colon occurs in a stepwise fashion. It begins with colonization of the mucin layer, which is followed by stimulation of a proinflammatory response that causes nonspecific tissue damage that may facilitate parasite invasion of the underlying colonic mucosa. Unfortunately, the parasite and/or host factors that stimulate a proinflammatory response in the gut are poorly understood. In this study, we found that live E. histolytica or secretory or proteins (SP) and soluble ameba components (SAP) can markedly increase interleukin-8 (IL-8) mRNA expression and protein production in colonic epithelial cells. The IL-8-stimulating molecule produced by live amebae was identified as prostaglandin E 2 (PGE 2 ) as trophozoites treated with cyclooxygenase inhibitors inhibited the biosynthesis of PGE 2 and eliminated IL-8 production induced by live parasites or ameba components. Moreover, using specific prostaglandin EP2 and EP4 receptor agonists and antagonists, we found that PGE 2 binds exclusively through EP4 receptors in colonic epithelial cells to stimulate IL-8 production. Silencing of EP4 receptors with EP4 small interfering RNA completely eliminated SP-and SAP-induced IL-8 production. These studies identified bioactive PGE 2 as a one of the major virulence factors produced by E. histolytica that can stimulate the potent neutrophil chemokine and activator IL-8, which can trigger an acute host inflammatory response. Thus, the induction of IL-8 production in response to E. histolytica-derived PGE 2 may be a mechanism that explains the initiation and amplification of acute inflammation associated with intestinal amebiasis.Entamoeba histolytica is an enteric protozoan parasite and the fourth leading cause of death due to a parasite (26). Humans are the only known host for E. histolytica, and about 50 million people are affected worldwide each year. The pathogenesis of amebiasis is believed to be a multistep and multifactorial process. Although a large number of studies have attempted to unravel the factors or molecules responsible for the pathogenesis of amebiasis, the processes involved in pathogenesis are not well understood. In most infected individuals, E. histolytica trophozoites exist as commensals. However, in a small percentage of infections, amebae can elude luminal and epithelial barrier host defense mechanisms and invade the intestinal mucosa, causing ulcers and amebic colitis. Even though host inflammatory responses play an important role in the onset and progression of invasive amebiasis, little is known about the parasite factors that initiate this event. Even less is known about the parasite components that are secreted or released in the gut and can modulate colonic epithelial cell functions.

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The Cys-Asn-Ser carboxyl-terminal end group is the pharmacophore of the amebic anti-inflammatory monocyte locomotion inhibitory factor (MLIF)

Cited by 13 publications

References 7 publications

Anti-inflammatory defense mechanisms of Entamoeba histolytica

Anti-inflammatory defense mechanisms of Entamoeba histolytica

Importance of asparagine on the conformational stability and chemical reactivity of selected anti-inflammatory peptides

Prostaglandin E₂Produced byEntamoeba histolyticaBinds to EP4 Receptors and Stimulates Interleukin-8 Production in Human Colonic Cells

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The Cys-Asn-Ser carboxyl-terminal end group is the pharmacophore of the amebic anti-inflammatory monocyte locomotion inhibitory factor (MLIF)

Cited by 13 publications

References 7 publications

Anti-inflammatory defense mechanisms of Entamoeba histolytica

Anti-inflammatory defense mechanisms of Entamoeba histolytica

Importance of asparagine on the conformational stability and chemical reactivity of selected anti-inflammatory peptides

Prostaglandin E2Produced byEntamoeba histolyticaBinds to EP4 Receptors and Stimulates Interleukin-8 Production in Human Colonic Cells

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Resources

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Prostaglandin E₂Produced byEntamoeba histolyticaBinds to EP4 Receptors and Stimulates Interleukin-8 Production in Human Colonic Cells