Wang Y, Liu B, Zhang J, Sun L, Wen W, Fan Q, Yi L
College of Animal Science and Technology, Henan University of Science and Technology, Luoyang, China.
Key Laboratory of Molecular Pathogen and Immunology of Animal of Luoyang, Luoyang, China.
Lett Appl Microbiol. 2019 Jul;69(1):11-15. doi: 10.1111/lam.13164.
Salmonella enterica serovar Typhimurium (S. Typhimurium) inhabits a wide range of hosts, including poultry, and causes acute gastroenteritis in humans that may result in death. Superoxide dismutase (SOD) is an important antioxidant enzyme present in nearly all living cells exposed to oxygen. Recently, we reported the novel roles of SOD in serum resistance and biofilm formation in S. Typhimurium. This study was designed to explore the effect of infection with sodA mutant of S. Typhimurium on the autophagic response of macrophages. Murine macrophage cell line RAW264·7 was infected with wild-type (LSM52), a sodA deletion mutant (LSM52ΔsodA) and complemented strain (LSM52CΔsodA). We found that sodA deletion triggered remarkable autophagic responses in infected cells, shown as higher concentrations of LC3-II or Beclin-1 than those infected with the wild-type or complemented strain during the first hour post-infection in S. Typhimurium. Consistent with these results, the number of viable bacteria in cells infected with the sodA mutant was significantly lower than those infected with wild-type or complemented strains at 1 h, 2 h and 3 h post-infection in S. Typhimurium. All results indicated that infection with sodA mutant of S. Typhimurium leads to up-regulation of autophagy in Raw264·7 macrophages. SIGNIFICANCE AND IMPACT OF THE STUDY: Autophagy plays an important role in Salmonella infection although the role of autophagy in Salmonella infection remains unclear. This study was designed to explore the effect of sodA on the autophagic response of macrophage. We found that infection with sodA mutant of Salmonella Typhimurium could lead to up-regulation of autophagy in Raw264·7 macrophages.
肠炎沙门氏菌鼠伤寒血清型（鼠伤寒沙门氏菌）可寄居于包括家禽在内的多种宿主，并可导致人类急性肠胃炎，甚至可能致死。超氧化物歧化酶（SOD）是一种重要的抗氧化酶，几乎存在于所有暴露于氧气的活细胞中。最近，我们报道了SOD在鼠伤寒沙门氏菌血清抗性和生物膜形成中的新作用。本研究旨在探讨鼠伤寒沙门氏菌sodA突变体感染对巨噬细胞自噬反应的影响。用野生型（LSM52）、sodA缺失突变体（LSM52ΔsodA）和互补菌株（LSM52CΔsodA）感染小鼠巨噬细胞系RAW264·7。我们发现，sodA缺失在感染细胞中引发了显著的自噬反应，表现为在鼠伤寒沙门氏菌感染后第1小时，感染sodA缺失突变体的细胞中LC3-II或Beclin-1的浓度高于感染野生型或互补菌株的细胞。与这些结果一致，在鼠伤寒沙门氏菌感染后1小时、2小时和3小时，感染sodA突变体的细胞中活菌数量显著低于感染野生型或互补菌株的细胞。所有结果表明，鼠伤寒沙门氏菌sodA突变体感染导致Raw264·7巨噬细胞中自噬上调。研究的意义和影响：尽管自噬在沙门氏菌感染中的作用尚不清楚，但自噬在沙门氏菌感染中起着重要作用。本研究旨在探讨sodA对巨噬细胞自噬反应的影响。我们发现，鼠伤寒沙门氏菌sodA突变体感染可导致Raw264·7巨噬细胞中自噬上调。
