Down Regulation of<i>Entamoeba histolytica</i>Virulence by Monoxenic Cultivation with<i>Escherichia coli</i>O55 Is Related to a Decrease in Expression of the Light (35-Kilodalton) Subunit of the Gal/GalNAc Lectin

Padilla‐Vaca, Felipe; Ankri, Serge; Bracha, Rivka; Koole, Lucy Anna; Mirelman, David

doi:10.1128/iai.67.5.2096-2102.1999

Cited by 77 publications

(30 citation statements)

References 42 publications

(58 reference statements)

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“…Virulence reduction following monoaxenic culture or culture in artificial media has been observed for Paramoeba invadens and E. histolytica . Virulence was restored for these species after passage through the target host (Jellett & Scheibling 1988; Padilla‐Vaca, Ankri, Bracha, Koole & Mirelman 1999). It is possible that involvement of a cryptic pathogen (e.g.…”

Section: Discussionmentioning

confidence: 99%

Experimental amoebic gill disease of Atlantic salmon, Salmo salar L.: further evidence for the primary pathogenic role of Neoparamoeba sp. (Page, 1987)

Adams

Nowak

2004

Journal of Fish Diseases

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Amoebic gill disease (AGD) has been attributed to infection by Neoparamoeba sp. The causal mechanisms for AGD lesion development and the primary pathogenic role of Neoparamoeba sp. require elucidation. Three groups of Atlantic salmon were exposed to viable gill isolated amoebae, to sonicated amoebae, or to sea water containing viable amoebae without direct contact with gill epithelia. Fish were removed 8 days post-exposure and the gills assessed histologically for AGD. AGD occurred only when fish were exposed to viable trophozoites. Consequently, in an accompanying experiment, infection was evaluated histologically at 12, 24 and 48 h post-exposure in three groups of salmon, one group being mechanically injured 12 h prior to exposure. A progressive host response and significant increase (P < 0.001) in the numbers of attached amoebae was apparent over the 48-h duration in undamaged hemibranchs in both treatment groups. There were no significant differences to mucous cell populations. Attachment of Neoparamoeba sp. to damaged gill filaments was significantly reduced (P < 0.05) by 48 h post-exposure. These data further confirm and describe the primary pathogenic role of Neoparamoeba sp. and the early host response in AGD. Preliminary evidence suggests that lesions resulting from physical gill damage are not preferentially colonized by Neoparamoeba sp.

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Section: Discussionmentioning

confidence: 99%

Experimental amoebic gill disease of Atlantic salmon, Salmo salar L.: further evidence for the primary pathogenic role of Neoparamoeba sp. (Page, 1987)

Adams

Nowak

2004

Journal of Fish Diseases

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“…It is likely that the glycoconjugate is galactose or N ‐acetylgalactosamine (Findlay 2001). As Padilla‐Vaca, Ankri, Bracha, Koole & Mirelman (1999) have shown that the glycoconjugate profile of the bacteria used as the nutritional lawn for cultured Entamoeba histolytica is crucial in deciding if the organism is to be pathogenic or not, similar studies are warranted for N. pemaquidensis. This mechanism may also be involved in the apparent preference of N. pemaquidensis for hyperplastic gill epithelium (Munday et al .…”

Section: Pathogenesismentioning

confidence: 99%

Gill disease of marine fish caused by infection with Neoparamoeba pemaquidensis

Munday

Zilberg

Findlay

2001

Journal of Fish Diseases

161

159

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Amoebic gill disease (AGD) of maricultured salmonids, turbot, Scophthalmus maximus (L.), European seabass, Dicentrarchus labrax (L.), and sharpsnout seabream, Diplodus puntazzo (Cetti), caused by Neoparamoeba pemaquidensis has been reported from Australia (Tasmania), Ireland, France, Chile, North America (Washington State and California) and Spain. Of the salmonids, Atlantic salmon, Salmo salar L., appears to be the most susceptible with rainbow trout, Oncorhynchus mykiss (Walbaum), also suffering signi®cant disease. Only minor outbreaks have been reported in coho, O. kisutch (Walbaum), and chinook salmon, O. tshawytscha (Walbaum). The disease now accounts for 10±20% of production costs of Atlantic salmon in Tasmania and has lead to temporary abandonment of culture of this species in parts of Spain. It is of lesser, but still signi®cant, importance in other countries. Much is known about the pathology of AGD but the pathophysiology of the disease is poorly understood. There is evidence that non-speci®c immunity is involved in ®sh acquiring resistance to AGD, but no unequivocal evidence exists for protection as a result of speci®c immune responses. To date, for salmonids, the only effective treatment for AGD is a freshwater bath. Control procedures based on modi®cation of management strategies have been minimal and virtually unresearched.

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“…9,10 Old papers reported that gut bacteria, such as O55 Escherichia coli and Shigella dysenteriae, directly affect on the virulence of E. histolytica in vitro experiments. [11][12][13] Also, it was known that disease severity of autoimmune diseases, such as inflammatory bowel diseases and rheumatoid, are highly influenced by the gut microbiome.- [14][15][16] However, effect of gut microbiome on host immune response to external pathogen are rarely investigated in previous studies.…”

Section: Severity Of Entamoeba Histolytica Infection and The Gut Micrmentioning

confidence: 99%

Learning from the research on amebiasis and gut microbiome: Is stimulation by gut flora essential for effective neutrophil mediated protection from external pathogens?

Watanabe

Petri

2018

Gut Microbes

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Amebiasis, caused by intestinal infection with Entamoeba histolytica, is one of the leading causes of parasite infection-related mortality and morbidity globally. Although its pathogenesis, including determinant factors of infection outcome, remains unclear, recent clinical data indicate that the gut microbiome plays a role in determining the severity of amebiasis. Recently, we investigated the effects of the gut microbiome on neutrophil mediated protection from E. histolytica infection using a mouse model. We identified that surface expression of CXCR2 on neutrophils was diminished in mice with dysbiosis, which resulted in decreased neutrophil recruitment to the infection site, allowing more aggressive intestinal tissue damage by E. histolytica. Our results indicated that oxidase activity during E. histolytica infection was also diminished after dysbiosis, consistent with the results from prior research. Thus, the gut microbiome plays an important role in regulating neutrophil phenotype when fighting against external pathogens.

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Down Regulation ofEntamoeba histolyticaVirulence by Monoxenic Cultivation withEscherichia coliO55 Is Related to a Decrease in Expression of the Light (35-Kilodalton) Subunit of the Gal/GalNAc Lectin

Cited by 77 publications

References 42 publications

Experimental amoebic gill disease of Atlantic salmon, Salmo salar L.: further evidence for the primary pathogenic role of Neoparamoeba sp. (Page, 1987)

Experimental amoebic gill disease of Atlantic salmon, Salmo salar L.: further evidence for the primary pathogenic role of Neoparamoeba sp. (Page, 1987)

Gill disease of marine fish caused by infection with Neoparamoeba pemaquidensis

Learning from the research on amebiasis and gut microbiome: Is stimulation by gut flora essential for effective neutrophil mediated protection from external pathogens?

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