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Special Issue Editors

Special Issue Information

Dear Colleagues,

Microbial pathogens can cause serious diseases of aquatic animals and the result of the battle between host and pathogens will determine the occurrence of diseases. On one hand, to fight against infections, aquatic animals have evolved complex defense systems, including innate immunity and adaptive immunity. On the other hand, pathogens also develop numerous strategies such as immune evasion to antagonize host defense responses. Fundamental knowledge on this topic is being applied to prevent infectious disease outbreaks and improve aquatic animal health. This Special Issue comprises high-quality original research articles and reviews, providing a comprehensive overview on the infectious diseases and immune defenses of aquatic animals. Highlight topics include host–pathogen interactions; cellular immune responses and signaling pathways; immune cells; cytokines and humoral factors; vaccination and disease resistance.

Prof. Dr. Xiuzhen Sheng
Prof. Dr. Li Lin
Guest Editors

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Related Special Issue

Published Papers (1 paper)

Research

16 pages, 4807 KiB

Open AccessArticle

The Role of the TLR4-MyD88 Signaling Pathway in the Immune Response of the Selected Scallop Strain “Hongmo No. 1” to Heat Stress

by Chenyang Yue, Kexin Zhang, Zhigang Liu, Wengang Lü, Hui Guo, Liqiang Zhao, Xinyu Song and James Kar-Hei Fang

Animals 2024, 14(3), 497; https://doi.org/10.3390/ani14030497 - 02 Feb 2024

Viewed by 843

Abstract

The innate immunity of marine bivalves is challenged upon exposure to heat stress, especially with increases in the frequency and intensity of heat waves. TLR4 serves a classical pattern recognition receptor in recognizing pathogenic microorganisms and activating immune responses. In this study, three genes, HMTLR4, HMMyD88 and HMTRAF6, were characterized as homologs of genes in the TLR4-MyD88 signaling pathway in the selected scallop strain “Hongmo No. 1”. According to RT-PCR, acute heat stress (32 °C) inhibited genes in the TLR4-MyD88 signaling pathway, and LPS stimulation-induced activation of TLR4-MyD88 signal transduction was also negatively affected at 32 °C. ELISA showed LPS-induced tumor necrosis factor alpha (TNF-α) or lysozyme (LZM) activity, but this was independent of temperature. RNA interference (RNAi) confirmed that HMTLR4 silencing suppressed the expression of its downstream gene, whether at 24 °C or at 32 °C. The level of TNF-α and the activity of LZM also decreased after injection with dsRNA, indicating a negative effect on the innate immunity of scallops. Additionally, acute heat stress affected the suppression of downstream gene expression when compared with that at 24 °C, which led us to the hypothesis that heat stress directly influences the downstream targets of HMTLR4. These results enrich the knowledge of scallop immunity under heat stress and can be beneficial for the genetic improvement of new scallop strains with higher thermotolerance. Full article

(This article belongs to the Special Issue Second Edition of Aquatic Animal Disease and Immunity)

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