Activation of Helicobacter pylori causes either autoimmune thyroid diseases or carcinogenesis in the digestive tract

Title:

Activation of Helicobacter pylori causes either autoimmune thyroid diseases or carcinogenesis in the digestive tract

Creator:

Jaromír Astl and Ivan Šterzl

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:83ae9cab-2697-4a73-9220-bdac25346e3b
uuid:83ae9cab-2697-4a73-9220-bdac25346e3b
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, mutageny, maligní nádorová onemocnění, mutagens, cancer, Helicobacter pylori, autoimmune thyroiditis, MELISA, CagA gene, Tonsillar tissue, Oropharynx, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Helicobacter pylori has been implicated in stimulation of immune system, development of autoimmune endocrinopathies as autoimmune thyroiditis (AT) and on other hand induction of immunosupresion activates gastric and extra-gastric diseases such as gastric ulcer or cancer. It causes persistent lifelong infection despite local and systemic immune response. Our results indicate that Helicobacter pylori might cause inhibition of the specific cellular immune response in Helicobacter pyloriinfected patients with or without autoimmune diseases such as AT. We cannot also declare the carcinogenic effect in oropharynx. However the association of any infection agents and cancerogenesis exists. The adherence of Helicobacter pylori expression and enlargement of benign lymphatic tissue and the high incidence of the DNA of Helicobacter pylori in laryngopharyngeal and oropharyngeal cancer is reality. LTT appears to be a good tool for detection of immune memory cellular response in patients with Helicobacter pylori infection and AT. All these complications of Helicobacter pylori infection can be abrogated by successful eradication of Helicobacter pylori., J. Astl, I. Šterzl., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false