Features of the human immune response to Helicobacter pylori infection

Abstract

Helicobacter pylori is considered the etiological agent of acute and chronic forms of gastritis, and is also capable of exerting a multifactorial effect on the host organism and on the nature of the immune response. The inflammatory response to H. pylori infection has its own characteristics. With an active course, inflammatory reactions, when the modulating effect of regulatory T-lymphocytes (T-reg) is weakened and populations of pro-inflammatory cells (T-helpers 1, 17, 22 type and follicular T-helpers) are activated, which have pronounced destructive changes in the gastric mucosa and the duodenum. guts. Macrophages, dendritic cells and neutrophils are cellular factors of the innate immune system, as well as adaptive immunity, which provides protection against infection. In turn, H. pylori uses a variety of mechanisms to evade the destruction of the host immune system. Long-term preservation of inflammation can cause local activation of mutagenesis, which initiates the development of malignant neoplasms of the gastric mucosa. A review of the host immune response to H. pylori is devoted to this analytical review.

Helicobacter pylori: clinical significance and diagnostic principles

“…Как только CagA фосфорилируется, запускаются процессы, приводящие к морфологическим изменениям клетки, а именно к нарушению цитоскелета эпителиоцитов. Фосфорилирование тирозиновыми протеинкиназами внутриклеточного CagA является важным этапом в канцерогенезе желудка [7,11].…”

Use of sodium polyprenylphosphate to correct changes in the immune response caused by Helicobacter pylori CagA proteins in the experiment

“…р.) обладают широким спектром патогенетически значимых факторов патогенности, обеспечивающих выживание и длительную персистенцию возбудителя в агрессивной среде желудочно-кишечного тракта (ЖКТ) [1,2 ].…”