Involvement of β2-integrin in ROS-mediated neutrophil apoptosis induced by Entamoeba histolytica

Sim, Seobo; Park, Soon‐Jung; Yong, Tai Soon; Im, Kyung Il; Shin, Myoung-Ho

doi:10.1016/j.micinf.2007.06.013

Cited by 30 publications

(24 citation statements)

References 27 publications

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“…Integrin is a typical adhesion molecule interacting with mammalian galectin [22]. Recently, we presented evidence that there might be a signaling association between β 2 integrin on human neutrophils and amoebic galectin in E. histolytica -induced host cell apoptosis [5]. Moreover, it remains a possibility that amoebic galectin might directly associate with glycosylated residues of NOX2 since human NOX2 (gp91 phox ) is a glycosylated protein, and the carbohydrate chains are largely composed of N-acetylglucosamine and galactose [23].…”

Section: Discussionmentioning

confidence: 99%

“…E. histolytica -induced colon cell death is crucial for provocation of neutrophil-mediated tissue inflammation in the amoeba-infected colon lesions [3]. Adherence of amoebae to host cells through amoebic gal-lectin and host β 2 -integrin induces host cell death in vitro [4,5]. Host cell death induced by E. histolytica does not involve either of the two common cell death signaling pathways of death receptors or mitochondria [6].…”

Section: Introductionmentioning

confidence: 99%

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Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

Kim

Lee

et al. 2013

Korean J Parasitol

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Entamoeba histolytica, which causes amoebic colitis and occasionally liver abscess in humans, is able to induce host cell death. However, signaling mechanisms of colon cell death induced by E. histolytica are not fully elucidated. In this study, we investigated the signaling role of NOX in cell death of HT29 colonic epithelial cells induced by E. histolytica. Incubation of HT29 cells with amoebic trophozoites resulted in DNA fragmentation that is a hallmark of apoptotic cell death. In addition, E. histolytica generate intracellular reactive oxygen species (ROS) in a contact-dependent manner. Inhibition of intracellular ROS level with treatment with DPI, an inhibitor of NADPH oxidases (NOXs), decreased Entamoeba-induced ROS generation and cell death in HT29 cells. However, pan-caspase inhibitor did not affect E. histolytica-induced HT29 cell death. In HT29 cells, catalytic subunit NOX1 and regulatory subunit Rac1 for NOX1 activation were highly expressed. We next investigated whether NADPH oxidase 1 (NOX1)-derived ROS is closely associated with HT29 cell death induced by E. histolytica. Suppression of Rac1 by siRNA significantly inhibited Entamoeba-induced cell death. Moreover, knockdown of NOX1 by siRNA, effectively inhibited E. histolytica-triggered DNA fragmentation in HT29 cells. These results suggest that NOX1-derived ROS is required for apoptotic cell death in HT29 colon epithelial cells induced by E. histolytica.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

Kim

Lee

et al. 2013

Korean J Parasitol

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“…Furthermore, neutrophil depletion in murine models of infection resulted in more severe ulceration of susceptible strains than of resistant strains (2). 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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“…One of these mechanisms is the inhibition of host cell apoptosis, although the anti-or proapoptotic mechanisms associated with T. gondii infection remain controversial (Sim et al 2007; Lalibert e and Carruthers 2008; Lüder et al 2009). …”

Section: Article In Pressmentioning

confidence: 99%

Galectin-3 plays a modulatory role in the life span and activation of murine neutrophils during early Toxoplasma gondii infection

Alves¹,

Silva²,

Azzolini³

et al. 2010

Immunobiology

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Involvement of β2-integrin in ROS-mediated neutrophil apoptosis induced by Entamoeba histolytica

Cited by 30 publications

References 27 publications

Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

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

Galectin-3 plays a modulatory role in the life span and activation of murine neutrophils during early Toxoplasma gondii infection

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Involvement of β2-integrin in ROS-mediated neutrophil apoptosis induced by Entamoeba histolytica

Cited by 30 publications

References 27 publications

Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

Entamoeba histolytica Induces Cell Death of HT29 Colonic Epithelial Cells via NOX1-Derived ROS

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

Galectin-3 plays a modulatory role in the life span and activation of murine neutrophils during early Toxoplasma gondii infection

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