title: Acute cold stress improved the transcription of pro-inflammatory cytokines of Chinese soft-shelled turtle against Aeromonas hydrophila.
abstract: Chinese soft-shelled turtle, Pelodiscus sinensis, is widely cultured in East and Southeast Asian countries. It frequently encounters the stress of abrupt temperature changes, which leads to mass death in most cases. However, the mechanism underlying the stress-elicited death remains unknown. We have suspected that the stress impaired the immune function of Chinese soft-shelled turtle, which could result in the mass death, as we noticed that there was a clinical syndrome of infection in dead turtles. To test our hypothesis, we first performed bioinformatic annotation of several pro-inflammatory molecules (IL-1β, TNFα, IL-6, IL-12β) of Chinese soft-shelled turtle. Then, we treated the turtles in six groups, injected with Aeromonas hydrophila before acute cold stress (25 °C) and controls, after acute cold stress (15 °C) and controls as well as after the temperature was restored to 25 °C and controls, respectively. Subsequently, real-time PCR for several pro-inflammatory cytokines (IL-1β, TNFα, IL-6, IL-12β, IL-8 and IFNγ) was performed to assess the turtle immune function in spleen and intestine, 24 hours after the injection. We found that the mRNA expression levels of the immune molecules were all enhanced after acute cold stress. This change disappeared when the temperature was restored back to 25 °C. Our results suggest that abrupt temperature drop did not suppress the immune function of Chinese soft-shelled turtle in response to germ challenge after abrupt temperature drop. In contrast, it may even increase the expression of various cytokines at least, within a short time after acute cold stress.
authors.affiliation: School of Life Science, Shanxi University, Taiyuan 030006, Shanxi Province, China.
authors.forename: Zuobing
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Ministry of Education Key Laboratory of Biodiversity Science and Ecological Engineering, College of Life Sciences, Beijing Normal University, Beijing 100875, China.
authors.forename: Bojian
authors.initials: B
authors.lastname: Chen
authors.affiliation: Ministry of Education Key Laboratory of Biodiversity Science and Ecological Engineering, College of Life Sciences, Beijing Normal University, Beijing 100875, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Yuan
authors.affiliation: Ministry of Education Key Laboratory of Biodiversity Science and Ecological Engineering, College of Life Sciences, Beijing Normal University, Beijing 100875, China. Electronic address: cjniu@bnu.edu.cn.
authors.forename: Cuijuan
authors.initials: C
authors.lastname: Niu
mesh_terms: D016980:Aeromonas hydrophila / Q000276:immunology* / Q000502:physiology; D000595:Amino Acid Sequence; D000818:Animals; D003080:Cold Temperature; D016207:Cytokines / Q000145:classification / Q000235:genetics / Q000276:immunology*; D054884:Host-Pathogen Interactions / Q000276:immunology; D018836:Inflammation Mediators / Q000276:immunology / Q000378:metabolism; D018664:Interleukin-12 / Q000145:classification / Q000235:genetics / Q000276:immunology; D053583:Interleukin-1beta / Q000145:classification / Q000235:genetics / Q000276:immunology; D015850:Interleukin-6 / Q000145:classification / Q000235:genetics / Q000276:immunology; D008969:Molecular Sequence Data; D010802:Phylogeny; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017386:Sequence Homology, Amino Acid; D013312:Stress, Physiological / Q000235:genetics / Q000276:immunology; D014158:Transcription, Genetic / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000145:classification / Q000235:genetics / Q000276:immunology; D014426:Turtles / Q000235:genetics / Q000276:immunology* / Q000382:microbiology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12
keywords: Acute cold stress; Aeromonas hydrophila; Chinese soft-shelled turtle; Pro-inflammatory cytokines