Quinteiro-Filho W M, Calefi A S, Cruz D S G, Aloia T P A, Zager A, Astolfi-Ferreira C S, Piantino Ferreira J A, Sharif S, Palermo-Neto J
Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil.
Neuroimmunomodulation Research Group, Department of Pathology, School of Veterinary Medicine, University of São Paulo, São Paulo, SP, Brazil.
Vet Immunol Immunopathol. 2017 Apr;186:19-28. doi: 10.1016/j.vetimm.2017.02.006. Epub 2017 Feb 27.
A high ambient temperature is a highly relevant stressor in poultry production. Heat stress (HS) has been reported to reduce animal welfare, performance indices and increase Salmonella susceptibility. Salmonella spp. are major zoonotic pathogen that cause over 1 billion of human infections worldwide annually. Therefore, the current study was designed to analyze the effect of heat stress on Salmonella infection in chickens through modulation of the immune responses. Salmonella Enteritidis was inoculated via gavage at one day of age (10cfu/mL). Heat stress 31±1°C was applied from 35 to 41 days of age. Broiler chickens were divided into the following groups of 12 chickens: control (C); heat stress (HS31°C); S. Enteritidis positive control (PC); and S. Enteritidis+heat stress (PHS31°C). We observed that heat stress increased corticosterone serum levels. Concomitantly heat stress decreased (1) the IgA and IFN-γ plasmatic levels; (2) the mRNA expression of IL-6, IL-12 in spleen and IL-1β, IL-10, TGF-β in cecal tonsils; (3) the mRNA expression of AvBD4 and AvBD6 in cecal tonsils; and (4) the mRNA expression of TLR2 in spleen and cecal tonsils of chickens infected with S. Enteritidis (PHS31°C group). Heat stress also increased Salmonella colonization in the crop and caecum as well as Salmonella invasion to the spleen, liver and bone marrow, showing a deficiency in the control of S. Enteritidis induced infection. Together, the present data suggested that heat stress activated hypothalamus-pituitary-adrenal (HPA) axis, as observed by the increase in the corticosterone levels, which in turn presumably decreases the immune system activity, leading to an impairment of the intestinal mucosal barrier and increasing chicken susceptibility to the invasion of different organs by S. Enteritidis .
高温环境是家禽生产中一个高度相关的应激源。据报道，热应激（HS）会降低动物福利、生产性能指标，并增加沙门氏菌易感性。沙门氏菌属是主要的人畜共患病原体，每年在全球导致超过10亿人感染。因此，本研究旨在通过调节免疫反应来分析热应激对鸡沙门氏菌感染的影响。1日龄时通过灌胃接种肠炎沙门氏菌（10cfu/mL）。在35至41日龄时施加31±1°C的热应激。将肉鸡分为以下每组12只鸡的组：对照组（C）；热应激组（HS31°C）；肠炎沙门氏菌阳性对照组（PC）；肠炎沙门氏菌+热应激组（PHS31°C）。我们观察到热应激会增加血清皮质酮水平。同时，热应激降低了：（1）IgA和IFN-γ血浆水平；（2）脾脏中IL-6、IL-12以及盲肠扁桃体中IL-1β、IL-10、TGF-β的mRNA表达；（3）盲肠扁桃体中AvBD4和AvBD6的mRNA表达；以及（4）感染肠炎沙门氏菌的鸡（PHS31°C组）脾脏和盲肠扁桃体中TLR2的mRNA表达。热应激还增加了嗉囊和盲肠中的沙门氏菌定植以及沙门氏菌向脾脏、肝脏和骨髓的侵袭，表明在控制肠炎沙门氏菌诱导的感染方面存在缺陷。总之，目前的数据表明热应激激活了下丘脑-垂体-肾上腺（HPA）轴，这可通过皮质酮水平的升高观察到，进而可能降低免疫系统活性，导致肠道黏膜屏障受损，并增加鸡对肠炎沙门氏菌侵袭不同器官的易感性。
