Trichomonas vaginalis perturbs the junctional complex in epithelial cells

Costa, Rosa Maria Esteves Moreira da; Souza, Wanderley de; Benchimol, Marlene; Alderete, John F.; Morgado‐Díaz, José Andrés

doi:10.1038/sj.cr.7290340

Cited by 55 publications

(34 citation statements)

References 52 publications

(46 reference statements)

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“…Moreover, these cytotoxic effects were dependent on a direct interaction of T. foetus with the intestinal epithelium and could not be recapitulated using T. foetus conditioned media alone. Although the focus of this study was not to fully characterize the mechanism of epithelial cell death induced by feline T. foetus, activation of apoptosis has also been described in human vaginal and Caco-2 epithelial cells following infection with T. vaginalis (24,25) and bovine vaginal and oviduct epithelial cells following infection with bovine T. foetus (26,27). Further work is needed to determine the exact signaling mechanisms of cell death induced by feline T. foetus.…”

Section: Discussionmentioning

confidence: 99%

Cysteine Protease Activity of Feline Tritrichomonas foetus Promotes Adhesion-Dependent Cytotoxicity to Intestinal Epithelial Cells

et al. 2014

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bTrichomonads are obligate protozoan parasites most renowned as venereal pathogens of the reproductive tract of humans and cattle. Recently, a trichomonad highly similar to bovine venereal Tritrichomonas foetus but having a unique tropism for the intestinal tract was recognized as a significant cause of colitis in domestic cats. Despite a high prevalence, worldwide distribution, and lack of consistently effective drugs for treatment of the infection, the cellular mechanisms of T. foetus pathogenicity in the intestinal tract have not been examined. The aims of this study were to determine the pathogenic effect of feline T. foetus on porcine intestinal epithelial cells, the dependence of T. foetus pathogenicity on adhesion of T. foetus to the intestinal epithelium, and the identity of mediators responsible for these effects. Using an in vitro coculture approach to model feline T. foetus infection of the intestinal epithelium, these studies demonstrate that T. foetus promotes a direct contact-dependent activation of intestinal epithelial cell apoptosis signaling and progressive monolayer destruction. Moreover, these pathological effects were demonstrated to be largely dependent on T. foetus cell-associated cysteine protease activity. Finally, T. foetus cysteine proteases were identified as enabling cytopathic effects by promoting adhesion of T. foetus to the intestinal epithelium. The present studies are the first to examine the cellular mechanisms of pathogenicity of T. foetus toward the intestinal epithelium and support further investigation of the cysteine proteases as virulence factors in vivo and as potential therapeutic targets for ameliorating the pathological effects of intestinal trichomonosis.

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Section: Discussionmentioning

confidence: 99%

Cysteine Protease Activity of Feline Tritrichomonas foetus Promotes Adhesion-Dependent Cytotoxicity to Intestinal Epithelial Cells

et al. 2014

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“…Some parasites, such as Giardia intestinalis and Trichomonas vaginalis, do not invade host cells but rather decrease the cellular permeability of CaCo-2 epithelial cells. This effect was determined by examining TEER upon modifying the junctional complex in epithelial cells because these parasites alter the distribution of the ZO-1 and ZO-2 proteins (da Costa et al, 2005;Maia-Brigagão et al, 2012). In contrast, coculture of E. histolytica with an enteric T-84 cell layer decreases the TEER by disrupting the TJ proteins via the dephosphorylation and degradation of ZO-1 (Leroy et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Disruption of MDCK cell tight junctions by the free-living amoeba Naegleria fowleri

et al. 2013

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Naegleria fowleri is the aetiological agent of primary amoebic meningoencephalitis. This parasite invades its host by penetrating the olfactory mucosa. However, the mechanism of epithelium penetration is not well understood. In the present study, we evaluated the effect of N. fowleri trophozoites and the non-pathogenic Naegleria gruberi on Madin-Darby canine kidney (MDCK) tight junction proteins, including claudin-1, occludin and ZO-1, as well as on the actin cytoskeleton. Trophozoites from each of the free-living amoeba species were co-cultured with MDCK cells in a 1 : 1 ratio for 1, 3, 6 or 10 h. Light microscopy revealed that N. fowleri caused morphological changes as early as 3 h post-infection in an epithelial MDCK monolayer. Confocal microscopy analysis revealed that after 10 h of co-culture, N. fowleri trophozoites induced epithelial cell damage, which was characterized by changes in the actin apical ring and disruption of the ZO-1 and claudin-1 proteins but not occludin. Western blot assays revealed gradual degradation of ZO-1 and claudin-1 as early as 3 h post-infection. Likewise, there was a drop in transepithelial electrical resistance that resulted in increased epithelial permeability and facilitated the invasion of N. fowleri trophozoites by a paracellular route. In contrast, N. gruberi did not induce alterations in MDCK cells even at 10 h post-infection. Based on these results, we suggest that N. fowleri trophozoites disrupt epithelial monolayers, which could enable their penetration of the olfactory epithelium and subsequent invasion of the central nervous system.

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“…Under iron‐rich conditions and upon contact with epithelial cells, trichomonads express and mobilize adhesin proteins to their cell surface 45, 55. At least one bovine T. foetus and five functionally diverse T. vaginalis adhesin proteins, named on the basis of their molecular weights ( T. foetus : Tf190; T. vaginalis : AP120, AP65, AP51, AP33, AP23) have been identified 48, 49, 56, 57.…”

Section: Pathogenesis Of Trichomonosismentioning

confidence: 99%

“…Most of the cytopathic effects of trichomonads appear to be initiated by adherence of the parasite to the epithelium. For example, adhesion of T. vaginalis to intestinal epithelial monolayers (Caco‐2) results in an increase in permeability that is associated with altered tight junction function 55. When T. vaginalis is used to infect vaginal epithelial cells or HeLa cell monolayers, the epithelial cells undergo detachment, lysis, and apoptosis.…”

Section: Pathogenesis Of Trichomonosismentioning

confidence: 99%

Mechanisms ofTritrichomonas foetusPathogenicity in Cats with Insights from Venereal Trichomonosis

Tolbert

Gookin

2016

Veterinary Internal Medicne

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Almost 20 years has passed since trichomonosis was first recognized as a potential cause of diarrhea in domestic cats. Despite progress in confirming disease causation, developing means for diagnosis, and identifying approaches to treatment of the infection, we still know very little about how this parasite causes diarrhea. With increasing recognition of resistance of trichomonosis to treatment with 5‐nitroimidazole drugs, new treatment strategies based on an understanding of disease pathogenesis are needed. In this review, lessons learned from the pathogenesis of venereal trichomonosis in people and cattle are applied to clinical observations of trichomonosis in cats in effort to generate insight into areas where further research may be beneficial.

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Trichomonas vaginalis perturbs the junctional complex in epithelial cells

Cited by 55 publications

References 52 publications

Cysteine Protease Activity of Feline Tritrichomonas foetus Promotes Adhesion-Dependent Cytotoxicity to Intestinal Epithelial Cells

Cysteine Protease Activity of Feline Tritrichomonas foetus Promotes Adhesion-Dependent Cytotoxicity to Intestinal Epithelial Cells

Disruption of MDCK cell tight junctions by the free-living amoeba Naegleria fowleri

Mechanisms ofTritrichomonas foetusPathogenicity in Cats with Insights from Venereal Trichomonosis

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