恒河猴急性幽门螺杆菌感染早期会诱导产生主要为Th1型的免疫反应。

A predominant Th1 type of immune response is induced early during acute Helicobacter pylori infection in rhesus macaques.

作者信息

Mattapallil J J, Dandekar S, Canfield D R, Solnick J V

机构信息

Department of Internal Medicine, Division of Infectious Diseases, University of California Davis, Davis, California 95616, USA.

出版信息

Gastroenterology. 2000 Feb;118(2):307-15. doi: 10.1016/s0016-5085(00)70213-7.

DOI:10.1016/s0016-5085(00)70213-7

PMID:10648459

Abstract

BACKGROUND & AIMS: The immune response of gastric T cells during acute Helicobacter pylori infection has not been previously characterized. The aim of this study was to delineate the phenotypic and functional responses of gastric T cells during acute H. pylori infection of rhesus macaques.

METHODS

Four monkeys were experimentally infected with H. pylori. Gastric biopsy specimens and peripheral blood samples were obtained 1 and 12 weeks after inoculation. Samples from 3 animals uninfected with H. pylori served as controls. The immunophenotypic changes and functional potential of CD4(+) and CD8(+) T cells in gastric mucosa and peripheral blood to produce cytokines (interleukin [IL]-2, IL-4, IL-13, interferon [IFN]-gamma, MIP-1beta, and tumor necrosis factor [TNF]-alpha) were determined at a single cell level using flow cytometry.

RESULTS

An increase in CD4(+) T cells occurred in the gastric mucosa during acute H. pylori infection as early as 1 week after infection. Acute infection was characterized by a predominantly T helper (Th)1 (IL-2 and IFN-gamma) and proinflammatory (TNF-alpha and MIP-1beta) type of cytokine response and the absence of a Th2 type of response.

CONCLUSIONS

A predominant Th1 type response was induced early during acute H. pylori infection and may contribute to the development of gastric disease.

摘要

背景与目的

此前尚未对急性幽门螺杆菌感染期间胃T细胞的免疫反应进行过特征描述。本研究的目的是描绘恒河猴急性幽门螺杆菌感染期间胃T细胞的表型和功能反应。

方法

对4只猴子进行幽门螺杆菌实验性感染。在接种后1周和12周获取胃活检标本和外周血样本。来自3只未感染幽门螺杆菌的动物的样本用作对照。使用流式细胞术在单细胞水平测定胃黏膜和外周血中CD4(+)和CD8(+) T细胞产生细胞因子（白细胞介素 [IL]-2、IL-4、IL-13、干扰素 [IFN]-γ、MIP-1β和肿瘤坏死因子 [TNF]-α）的免疫表型变化和功能潜力。