Anti-<i>Anisakis</i> antibodies in colon cancer patients and their relationship with ?d T-cells

Many pathogens are related to carcinogenesis. Chronic inflammation, as a result of persistent infection, leads to DNA damage, higher expression of oncogenes, decreased apoptosis and immunosuppression, which are some of the reasons for cancer induction. Among parasites, Schistosoma, Opistorchis and C...

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Detalles Bibliográficos
Autores: Andreu-Ballester JC, Cuéllar C, Colmena-Zaragoza J, Galindo-Regal L, Hurtado-Marcos C, González-Fernández J, Balciscueta Z, García-Ballesteros C, López-Chuliá F, Jiménez AI, Llombart-Cussac A
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
País:España
Institución:Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana (FISABIO)
Repositorio:r-FISABIO. Repositorio Institucional de Producción Científica
OAI Identifier:oai:fisabio.fundanetsuite.com:p17013
Acceso en línea:https://fisabio.portalinvestigacion.com/publicaciones/17013
Access Level:acceso abierto
Palabra clave:Anisakis
Colon cancer
Specific antibodies
alpha beta T-cells
gamma delta T-cells
Apoptosis
Descripción
Sumario:Many pathogens are related to carcinogenesis. Chronic inflammation, as a result of persistent infection, leads to DNA damage, higher expression of oncogenes, decreased apoptosis and immunosuppression, which are some of the reasons for cancer induction. Among parasites, Schistosoma, Opistorchis and Clonorchis are recognised as infectious agents which contribute to cancer. A relationship between Anisakis and cancer was hypothesised because cellular responses to Anisakis products could result in inflammation and DNA damage. Previous research has shown a decrease in CD8+ gamma delta T-cells and an increase in alpha beta and gamma delta T-cell apoptosis in colon cancer (CC) samples. Ninety-two CC patients and 60 healthy subjects were recruited. gamma delta and alpha beta T-cells were analysed, and their apoptosis was evaluated. Anti-Anisakis antibodies were tested in sera from CC patients and controls. Anti-Anisakis IgG, IgM, IgA and IgE antibodies were significantly higher in CC patients. A significant increase in anti-Anisakis IgA levels was observed in patients with angiolymphatic invasion. The number of all gamma delta T-cells, as well as CD3+ CD4+ alpha beta T-cells, was significantly lower in CC patients. The apoptosis of all T-cells was significantly increased in patients with CC. We observed a significantly higher percentage of anti-Anisakis IgE positive patients having a deficit of CD3+ gamma delta T-cells. Our results suggest a relationship between Anisakis and CC.