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评价凝集素 PEIII-LC3-KDEL3 嵌合蛋白作为抗阿米巴肝脓肿疫苗候选物。

Evaluation of the PEIII-LC3-KDEL3 Chimeric Protein of Lectin as a Vaccine Candidate against Amebic Liver Abscess.

机构信息

Departamento de Morfología, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, C. P. 20131., Aguascalientes, Ags., Mexico.

Departamento de Química, Centro de Ciencias Básicas, Universidad Autónoma de Aguascalientes, C. P. 20131., Aguascalientes, Ags., Mexico.

出版信息

J Immunol Res. 2021 Mar 20;2021:6697900. doi: 10.1155/2021/6697900. eCollection 2021.

DOI:10.1155/2021/6697900
PMID:33824880
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8007359/
Abstract

is an intestinal parasite that causes dysentery and amebic liver abscess. 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 PEIII-LC3-KDEL3 recombinant protein. , this candidate vaccine inhibited adherence of 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. PEIII-LC3-KDEL3 reduced the expression of TNF-, IL-1, and NF-B in all immunized groups at 4- and 7-day postinfection. The levels of IL-10, FOXP3, and IFN- were elevated at 7 days. The immunohistochemistry assay confirmed this result, revealing an elevated quantity of +IFN- cells in the liver tissue. ALA formation in hamsters immunized was minimal, and few trophozoites were identified. Hence, immunization with PEIII-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.

摘要

是一种肠道寄生虫，可引起痢疾和阿米巴肝脓肿。具有通过毒力因子 Gal/GalNAc 凝集素结合宿主组织的能力；该分子诱导粘附抑制抗体反应，并防止阿米巴肝脓肿（ALA）。本工作显示了用 PEIII-LC3-KDEL3 重组蛋白免疫的效果。，该候选疫苗抑制滋养体与 HepG2 细胞单层的粘附，避免细胞溶解，并在仓鼠模型中观察到对组织肝损伤和不受控制的炎症的疫苗诱导保护。PEIII-LC3-KDEL3 在感染后 4 天和 7 天降低了所有免疫组中 TNF-、IL-1 和 NF-B 的表达。IL-10、FOXP3 和 IFN-的水平在第 7 天升高。免疫组织化学分析证实了这一结果，显示肝组织中 IFN-阳性细胞的数量增加。免疫仓鼠的 ALA 形成最小，鉴定出的滋养体很少。因此，用 PEIII-LC3-KDEL3 免疫可预防侵袭性阿米巴病，避免急性促炎反应，并在短时间内激活保护性反应。最后，该重组蛋白诱导血清 IgG 增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/30f954102766/JIR2021-6697900.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/834b4d2d25a5/JIR2021-6697900.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/0b90253babc1/JIR2021-6697900.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/f1126a4995ac/JIR2021-6697900.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/3d37e2fbacd9/JIR2021-6697900.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/bae4c78c1ef5/JIR2021-6697900.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/cbe0e185f6fc/JIR2021-6697900.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/85416467bba9/JIR2021-6697900.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/9747d233e632/JIR2021-6697900.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/30f954102766/JIR2021-6697900.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/834b4d2d25a5/JIR2021-6697900.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/0b90253babc1/JIR2021-6697900.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/f1126a4995ac/JIR2021-6697900.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/3d37e2fbacd9/JIR2021-6697900.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/bae4c78c1ef5/JIR2021-6697900.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/cbe0e185f6fc/JIR2021-6697900.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/85416467bba9/JIR2021-6697900.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/9747d233e632/JIR2021-6697900.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023d/8007359/30f954102766/JIR2021-6697900.009.jpg

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