巨噬细胞-γδT细胞免疫轴在猪格拉瑟氏病发病机制中的作用

doi:10.11843/j.issn.0366-6964.2018.05.002

摘要/Abstract

摘要：

副猪嗜血杆菌是存在于世界各主要养猪国家的一种重要细菌性病原体。仔猪出生不久便可通过接触致使细菌在上呼吸道寄居，并于一定条件下发病，临床感染可导致全身系统性炎症，其中以格拉瑟氏病为典型特征；该菌还可与猪其他重大细菌性和病毒性病原体混合感染，严重削弱猪群的免疫保护能力、极大影响生产效率。最近十多年，针对该菌的研究被持续关注，尤其在预防治疗和体内外感染模型建立的基础领域进展明显；但截至目前，人们对该细菌与宿主互作分子机制的相关认识还比较模糊，有待深入探讨。结合课题组自身研究和国内外其他主要发现，笔者认为：巨噬细胞（MΦ）-γδT细胞免疫轴可能在副猪嗜血杆菌感染的致病机制中处于主导地位；为此，本文拟针对这一观点展开论述，同时也希望借此文与国内同行深入切磋以增进科学认识。本文最终旨在梳理猪格拉瑟氏病发病机制中宿主免疫应答的主线、揭示猪机体参与感染的主要细胞组分，为今后相关分子信号研究和猪群Hps抗性品质改善的遗传素材挖掘提供新的研究视角。

Abstract:

Haemophilus parasuis (Hps) is a major bacterial pathogen in pigs that is prevalent in many countries worldwide. It can easily parasitize the upper respiratory tract of newborn piglets through contact transmission. Under certain conditions, Hps infection leads to systematic inflammations, in which the most typical clinical symptom is the so-called Glässer's disease. Co-infections of Hps with other bacteria and/or viruses have been reported, which can impair the host protective immunity and affect the production efficiency seriously. In the last decade, Hps infection has continuously attracted scientists and great progress in the basic research fields of prevention, control, and in vivo/in vitro challenges have been made. Whereas the molecular mechanism of Hps and host interaction is still fuzzy that warrants further investigation. Based on our studies and results from other teams, we speculate that the "Macrophage (MΦ)-γδT cell" immune axis may play a crucial role in the pathogenesis of Glässer's disease. In order to discuss better with our academic faculties, we herein present a deep review on this hypotheses. Objectives of this article are to discuss key issues of host immune response and to discover the underlying main cellular players. We hope to provide insight for the signaling pathway studies and Hps resistant genetic marker discoveries in pigs.

中图分类号:

程蕾, 陈洪波. 巨噬细胞-γδT细胞免疫轴在猪格拉瑟氏病发病机制中的作用[J]. 畜牧兽医学报, 2018, 49(5): 879-886.

CHENG Lei, CHEN Hong-bo. The Role of Macrophage-γδ T Cell Immune Axis in the Pathogenesis of Glässer's Disease[J]. ACTA VETERINARIA ET ZOOTECHNICA SINICA, 2018, 49(5): 879-886.

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