Amebic Colitis

Carolina, María; Escudero-Sepulveda, Andres; Alfonso, Juan Bruno Zayas

doi:10.5772/25453

Colitis 2012

DOI: 10.5772/25453

|View full text |Cite

Amebic Colitis

María Carolina¹,

Andres Escudero-Sepulveda²,

Juan Bruno Zayas Alfonso³

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2023

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

(1 citation statement)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…E. histolytica infection is usually asymptomatic; the parasite remains in the intestinal lumen, feeding on bacteria and host cells; however, in some cases, depending on the virulence of the strain and the type of host immune response can trigger severe tissue damage promoted by the invasion process as amoebic colitis, fulminant colitis or toxic colon and liver abscesses (Taherian et al, 2022).…”

mentioning

confidence: 99%

The Gal/GalNac lectin as a possible acetylcholine receptor in Entamoeba histolytica

Pacheco-Sánchez,

Martínez-Hernández,

Muñoz-Ortega

et al. 2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Entamoeba histolytica (E. histolytica) is a protozoan responsible for intestinal amebiasis in at least 500 million people per year, although only 10% of those infected show severe symptoms. It is known that E. histolytica captures molecules released during the host immune response through membrane receptors that favor its pathogenetic mechanisms for the establishment of amebic invasion. It has been suggested that E. histolytica interacts with acetylcholine (ACh) through its membrane. This promotes the increase of virulence factors and diverse mechanisms carried out by the amoeba to produce damage. The aim of this study is to identify a membrane receptor in E. histolytica trophozoites for ACh. Methods included identification by colocalization for the ACh and Gal/GalNAc lectin binding site by immunofluorescence, western blot, bioinformatic analysis, and quantification of the relative expression of Ras 5 and Rab 7 GTPases by RT-qPCR. Results show that the Gal/GalNAc lectin acts as a possible binding site for ACh and this binding may occur through the 150 kDa intermediate subunit. At the same time, this interaction activates the GTPases, Ras, and Rab, which are involved in the proliferation, and reorganization of the amoebic cytoskeleton and vesicular trafficking. In conclusion, ACh is captured by the parasite, and the interaction promotes the activation of signaling pathways involved in pathogenicity mechanisms, contributing to disease and the establishment of invasive amebiasis.

show abstract

mentioning

confidence: 99%

The Gal/GalNac lectin as a possible acetylcholine receptor in Entamoeba histolytica

Pacheco-Sánchez,

Martínez-Hernández,

Muñoz-Ortega

et al. 2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

hi@scite.ai

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Amebic Colitis

Cited by 1 publication

References 10 publications

The Gal/GalNac lectin as a possible acetylcholine receptor in Entamoeba histolytica

The Gal/GalNac lectin as a possible acetylcholine receptor in Entamoeba histolytica

Contact Info

Product

Resources

About