scholarly journals Evaluation of the PEΔIII-LC3-KDEL3 Chimeric Protein of Entamoeba histolytica-Lectin as a Vaccine Candidate against Amebic Liver Abscess

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Sandra L. Martínez-Hernández ◽  
Viridiana M. Becerra-González ◽  
Martín H. Muñoz-Ortega ◽  
Víctor M. Loera-Muro ◽  
Manuel E. Ávila-Blanco ◽  
...  

Entamoeba histolytica is an intestinal parasite that causes dysentery and amebic liver abscess. E. histolytica has the capability to invade host tissue by union of virulence factor Gal/GalNAc lectin; this molecule induces an adherence-inhibitory antibody response as well as to protect against amebic liver abscess (ALA). The present work showed the effect of the immunization with PEΔIII-LC3-KDEL3 recombinant protein. In vitro, this candidate vaccine inhibited adherence of E. histolytica trophozoites to HepG2 cell monolayer, avoiding the cytolysis, and in a hamster model, we observed a vaccine-induced protection against the damage to tissue liver and the inhibition of uncontrolled inflammation. PEΔIII-LC3-KDEL3 reduced the expression of TNF-α, IL-1β, and NF-κB in all immunized groups at 4- and 7-day postinfection. The levels of IL-10, FOXP3, and IFN-γ were elevated at 7 days. The immunohistochemistry assay confirmed this result, revealing an elevated quantity of +IFN-γ cells in the liver tissue. ALA formation in hamsters immunized was minimal, and few trophozoites were identified. Hence, immunization with PEΔIII-LC3-KDEL3 herein prevented invasive amebiasis, avoided an acute proinflammatory response, and activated a protective response within a short time. Finally, this recombinant protein induced an increase of serum IgG.

2000 ◽  
Vol 68 (1) ◽  
pp. 400-402 ◽  
Author(s):  
Karl B. Seydel ◽  
Sara J. Smith ◽  
Samuel L. Stanley

ABSTRACT Evidence from in vitro studies suggests that gamma interferon (IFN-γ) and nitric oxide (NO) are important in host defense against the protozoan parasite Entamoeba histolytica. We used SCID mice with targeted disruption of the IFN-γ receptor gene and mice with targeted disruption of the gene encoding inducible NO synthase to show that IFN-γ plays a role in the innate immunity to amebic liver abscess seen in SCID mice while NO is required for control of amebic liver abscess in immunocompetent mice.


2001 ◽  
Vol 87 (1) ◽  
pp. 49-56 ◽  
Author(s):  
J. Pacheco-Yépez ◽  
R. Campos-Rodríguez ◽  
M. Shibayama ◽  
J. Ventura-Juárez ◽  
J. Serrano-Luna ◽  
...  

PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 595-598
Author(s):  
Mary Ellen Rimsza ◽  
Robert A. Berg

An infant with cutaneous amebiasis of the vulva and amebic liver abscess is described. Epidemiologic investigations and serologic studies were crucial in establishing the diagnosis. The vulvar amebic ulcers responded dramatically to metronidazole therapy. Cutaneous amebiasis is a rare complication of Entamoeba histolytica infection which should be considered in the differential diagnosis of perineovulvar or penile ulcers. Cutaneous amebiasis may also occur on the abdominal wall surrounding a draining hepatic abscess, colostomy site, or laparotomy incision.


2015 ◽  
Vol 2015 ◽  
pp. 1-3 ◽  
Author(s):  
Devon McKenzie ◽  
Michael Gale ◽  
Sunny Patel ◽  
Grazyna Kaluta

Even in the absence of Amebic colitis, Amebic liver abscess (ALA) is the most common extraintestinal complication ofEntamoeba histolyticainfection. In the USA, it is most prevalent in middle aged immigrant males from endemic countries such as Africa, Mexico, and India. One of the complications of ALA is inferior vena cava (IVC) thrombosis, which is believed to result from the mechanical compression of the IVC and the consequent thrombogenic nidus elicited from the resultant inflammatory response. There are very few reported cases and even fewer in which the thrombus became a harbinger to pulmonary thromboembolism. We present the case of a 43-year-old male from West Africa who presented with the chief complaint of right upper quadrant abdominal pain for one week associated with persistent nonproductive cough. He had a positive serumEntamoeba histolyticaantibody with CT scan findings of a hepatic abscess with thrombosis of the hepatic vein and inferior vena cava and numerous bilateral pulmonary emboli. This amebic liver abscess was successfully treated with metronidazole and paromomycin, whereas the pulmonary thromboembolism was managed with medical anticoagulation. Based on current knowledge, this is the first reported case in the USA.


2007 ◽  
Vol 76 (1) ◽  
pp. 161-169 ◽  
Author(s):  
René E. Vasquez ◽  
Lijun Xin ◽  
Lynn Soong

ABSTRACT Leishmania amazonensis can cause progressive disease in most inbred strains of mice. We have previously reported that treatment with CXCL10 activates macrophage (MΦ) effector function(s) in parasite killing and significantly delays lesion development in susceptible C57BL/6 mice via enhanced gamma interferon (IFN-γ) and interleukin 12 (IL-12) secretion; however, the mechanism underlying this enhanced immunity against L. amazonensis infection remains largely unresolved. In this study, we utilized stationary promastigotes to infect bone marrow-derived dendritic cells (DCs) of C57BL/6 mice and assessed the activation of DC subsets and the capacity of these DC subsets to prime CD4+ T cells in vitro. We found that CXCL10 induced IL-12 p40 production but reduced IL-10 production in uninfected DCs. Yet L. amazonensis-infected DCs produced elevated levels of IL-10 despite CXCL10 treatment. Elimination of endogenous IL-10 led to increased IL-12 p40 production in DCs as well as increased proliferation and IFN-γ production by in vitro-primed CD4+ T cells. In addition, CXCL10-treated CD4+ T cells became more responsive to IL-12 via increased expression of the IL-12 receptor β2 chain and produced elevated levels of IFN-γ. This report indicates the utility of CXCL10 in generating a Th1-favored, proinflammatory response, which is a prerequisite for controlling Leishmania infection.


2004 ◽  
Vol 72 (2) ◽  
pp. 678-683 ◽  
Author(s):  
Xiaochun Zhang ◽  
Zhi Zhang ◽  
Diane Alexander ◽  
Rivka Bracha ◽  
David Mirelman ◽  
...  

ABSTRACT Entamoeba histolytica trophozoites produce amoebapores, a family of small amphipathic peptides capable of insertion into bacterial or eukaryotic membranes and causing cellular lysis. Recently, E. histolytica trophozoites that are totally deficient in the production of amoebapore-A were created through a gene silencing mechanism (R. Bracha, Y. Nuchamowitz, and D. Mirelman, Eukaryot. Cell 2:295-305, 2003). Here we tested the virulence of amoebapore A(−) trophozoites in models of the two major forms of amebic disease: amebic liver abscess and amebic colitis. We demonstrate that amoebapore expression is required for full virulence in the SCID mouse model of amebic liver abscess, but E. histolytica trophozoites that do not express amoebapore-A can still cause inflammation and tissue damage in infected human colonic xenografts. These data are consistent with the concept that tissue damage may proceed by different mechanisms in amebic liver abscess compared to amebic colitis.


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