Hashemi Shabnam, Hosseini Seyed Masoud, Ghalyanchilangeroudi Arash, Sheikhi Nariman
Department of Microbiology and Microbial Biotechnology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University, Tehran, Iran.
Department of Microbiology and Immunology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
Iran J Microbiol. 2021 Feb;13(1):17-22. doi: 10.18502/ijm.v13i1.5487.
Infection with Infectious bronchitis virus (IBV) and avian pathogenic (APEC) is an important respiratory infection worldwide. Apoptosis is a physiological process of cell death that occurs as part of normal development and responds to a variety of physiological and pathophysiological stimuli. The identification of molecular mechanisms of action or inaction of key apoptotic proteins is important. This study aimed to investigate apoptotic related genes in the trachea tissue of infected (IBV variant 2, and APEC serotype O78: K80) SPF chickens group compared to the control group.
Forty SPF chickens was divided into 2 groups. Differential transcriptional profile in the infected SPF chickens trachea tissue was compared to those of control group in the early stage of infection by Illumina RNA-seq technique paired-end and strand-specific sequencing. Differentially expressed genes (DEGs) of transcriptome profiling of the trachea from the infected group were identified. Gene ontology category, KEGG pathway, and STRING analysis were analyzed to identify relationships among differentially expressed genes.
Twenty-eight apoptotic genes were identified. They consisted of six pathways related to cell death: the extrinsic pathway, intrinsic pathway, endoplasmic reticulum stress pathway, MAPK signaling pathway, and cell death by NFkB and activates mTOR pathway and some regulator and apoptosis inhibitors.
All of the apoptotic genes in our study were up-regulated. Among these genes, the more fold change value was for TRADD and BCL2A1 genes, and the less fold change value was for MAP3K14, NFKB1, PIK3CB, and ITPR2 genes.
感染传染性支气管炎病毒（IBV）和禽致病性大肠杆菌（APEC）是全球范围内一种重要的呼吸道感染。细胞凋亡是细胞死亡的生理过程，是正常发育的一部分，并对多种生理和病理生理刺激作出反应。确定关键凋亡蛋白的作用或无作用的分子机制很重要。本研究旨在调查感染（IBV变异株2和APEC血清型O78:K80）的SPF鸡组与对照组相比气管组织中的凋亡相关基因。
40只SPF鸡分为2组。通过Illumina RNA-seq技术的双末端和链特异性测序，比较感染的SPF鸡气管组织与对照组在感染早期的差异转录谱。鉴定感染组气管转录组谱的差异表达基因（DEGs）。分析基因本体类别、KEGG通路和STRING分析，以确定差异表达基因之间的关系。
鉴定出28个凋亡基因。它们由六个与细胞死亡相关的途径组成：外源性途径、内源性途径、内质网应激途径、MAPK信号通路以及通过NFkB的细胞死亡和激活mTOR途径以及一些调节因子和凋亡抑制剂。
本研究中所有凋亡基因均上调。在这些基因中，TRADD和BCL2A1基因的倍数变化值较大，而MAP3K14、NFKB1、PIK3CB和ITPR2基因的倍数变化值较小。
