Journal
SCIENCE OF THE TOTAL ENVIRONMENT
Volume 912, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.scitotenv.2023.168758
Keywords
Largemouth Bass; Heat exposure; Aeromonas hydrophila; Heat-induced disease susceptibility; Metabolic pathway shift
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This study investigates the effects of heat exposure on oxidative and immune indices in Largemouth Bass (LMB) and reveals that chronic heat exposure induces oxidative stress, impairs immune function, and increases susceptibility to bacterial infection. RNA sequencing analysis further reveals the gene expression changes associated with chronic heat exposure and bacterial infection, shedding light on the underlying mechanisms.
Aquaculture of Largemouth Bass (LMB, Micropterus salmoides), an economically important species, is badly affected by the outbreak of bacterial diseases in summer. However, the mechanisms underlying heat-induced disease susceptibility remain largely unknown. In this study, after exposure to 34 C-degrees for 1, 7 and 14 d, the head kidney, spleen and blood of LMB were sampled for biochemical and histological assays to explore the effects of heat exposure on the oxidative and immunological indices. Compared to the controls maintained at 28 C-degrees, chronic heat exposure (34 C-degrees for 14 d) induced oxidative stress, caused cell apoptosis and decreased expression of the immunological genes in the head kidney and spleen tissues; and attenuated the blood immunological indices. Consistent with the impaired immunological functions, chronic heat exposure predisposed LMB to Aeromonas hydrophila infection and significantly (p < 0.001) increased tissue bacterial load. Furthermore, the effects of chronic heat exposure (heat), A. hydrophila infection (infection) and heat exposure followed by A. hydrophila infection (heat + infection) on gene expression in the head kidney and spleen of LMB were characterized by RNA sequencing. The results indicated that chronic heat exposure facilitated the bacteria-elicited changes in expression of the genes involved in a couple of metabolic and signaling pathways in both tissues. Upon heat + infection, the pathways involved in energy production and nutrients biosynthesis were enhanced, whereas those associated with the host cell functions such as cell-cell interactions and cell signaling were depressed. Our data provide new insights into the mechanisms underlying heat-induced disease susceptibility in LMB.
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