阿米巴病是由溶组织内阿米巴引起的疾病,影响人类的大肠,偶尔导致肠外病变。Entamoebadispar是另一种被认为是共生的变形虫,虽然它已被发现在患者表现为肠道失调性结肠炎和非肠道结肠炎,还有阿米巴肝脓肿.阿米巴毒力因子对病变的侵袭和发展至关重要。有证据表明,肠杆菌与滋养体的关联有助于阿米巴毒力因子的基因表达增加。肠致病性大肠杆菌是引起腹泻的重要细菌,在世界人口中发病率很高,允许它与Entamoebasp交互。在同一主机。在这种情况下,本研究旨在通过量化毒力因子的基因表达来评估肠致病性大肠杆菌对ACFN和ADOEntamoebadispar菌株的影响,包括半乳糖/N-乙酰基-D-半乳糖胺结合凝集素,半胱氨酸蛋白酶2和变形虫A和C。该研究评估了阿米巴肝脓肿的进展和形态学方面以及炎性细胞的分布。我们的结果表明,EPEC和ACFN之间的相互作用能够增加毒力因子的基因表达,以及病变面积和炎症浸润的活性。然而,与ADO菌株的关联并不影响毒力因子的基因表达。一起,我们的研究结果表明,EPEC之间的相互作用,ACFN,和ADOEntamoebadispar菌株导致Gal/GalNAc结合凝集素和CP2的体外和体内基因表达差异,NAG,EPO,因此,导致病变的能力。
Amoebiasis is a disease caused by Entamoeba histolytica, affecting the large intestine of humans and occasionally leading to extra-intestinal lesions. Entamoeba dispar is another amoeba species considered commensal, although it has been identified in patients presenting with dysenteric and nondysenteric colitis, as well as amoebic liver abscess. Amoebic virulence factors are essential for the invasion and development of lesions. There is evidence showing that the association of enterobacteria with trophozoites contributes to increased gene expression of amoebic virulence factors. Enteropathogenic Escherichia coli is an important bacterium causing diarrhea, with high incidence rates in the world population, allowing it to interact with Entamoeba sp. in the same host. In this context, this study aims to evaluate the influence of enteropathogenic Escherichia coli on ACFN and ADO Entamoeba dispar strains by quantifying the gene expression of virulence factors, including galactose/N-acetyl-D-galactosamine-binding lectin, cysteine proteinase 2, and amoebapores A and C. Additionally, the study assesses the progression and morphological aspect of amoebic liver abscess and the profile of inflammatory cells. Our results demonstrated that the interaction between EPEC and ACFN Entamoeba dispar strains was able to increase the gene expression of virulence factors, as well as the lesion area and the activity of the inflammatory infiltrate. However, the association with the ADO strain did not influence the gene expression of virulence factors. Together, our findings indicate that the interaction between EPEC, ACFN, and ADO Entamoeba dispar strains resulted in differences in vitro and in vivo gene expression of Gal/GalNAc-binding lectin and CP2, in enzymatic activities of MPO, NAG, and EPO, and consequently, in the ability to cause lesions.