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Antibiotics
Special Issues
Bacterial Infection and PRRs-Mediated Innate Immune Responses in Fish
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Bacterial Infection and PRRs-Mediated Innate Immune Responses in Fish

A special issue of Antibiotics (ISSN 2079-6382). This special issue belongs to the section "Antibiotics in Animal Health".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 7327

Special Issue Editors

Prof. Dr. Mingxian Chang

E-Mail Website
Guest Editor
Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China
Interests: innate immune recognition; pathogen-host interaction; anti-infective immunity; immune escape
Prof. Dr. Jianguo Su

E-Mail Website
Guest Editor
Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan 430070, China
Interests: antimicrobial peptide; hepcidin; defensin; interferon; chemokine; toll-like receptor; aquatic animal

Special Issue Information

Dear Colleagues,

The innate immune system is able to recognize a large variety of pathogens through different families of pattern recognition receptors (PRRs), which are often conserved among plants, invertebrates and vertebrates. In teleost fish, the identified PRRs include Toll-like receptors (TLRs), peptidoglycan recognition proteins (PGRPs), NOD-like receptors (NLRs), retinoic acid-inducible gene-I-like receptors (RLRs), scavenger receptors (SRs) and C-type lectin receptors (CLRs). Compared with those homologues from higher vertebrates, increasing evidence has demonstrated that piscine PRRs and those effector molecules involved in PRR-mediated signaling pathways undergo diverse alternative splicing, gene duplication or gene expansion. Understanding how these PRRs and effector molecules contribute to regulate immune response during bacterial infection or maintain immune homeostasis will be essential to devise strategies to intervene infectious diseases in teleost fish. This Special Issue seeks manuscript submissions that further enhance our understanding of exploring pattern recognition by these PRRs, induced signaling pathways by these PRRs, cross-talks between these PRRs and effector functions mediated by these PRRs in response to bacterial infections. It also aims to address the roles of innate effector molecules involved in PRR-mediated signaling pathways, which cover, but are not limited to, antimicrobial peptides and cytokines.

Prof. Dr. Mingxian Chang
Prof. Dr. Jianguo Su
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antibiotics is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pattern recognition receptors
  • antimicrobial effector molecules
  • PRRs-mediated signaling pathways
  • immune regulation
  • bacterial infection

Published Papers (3 papers)

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Research

16 pages, 6825 KiB  
Article
RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea
by Pengfei Zou, Kaiqing Li, Ying Li, Yingjia Shen, Ziping Zhang and Yilei Wang
Antibiotics 2021, 10(10), 1199; https://doi.org/10.3390/antibiotics10101199 - 1 Oct 2021
Cited by 5 | Viewed by 1935
Abstract
Receptor-interacting protein 3 (RIP3) has been demonstrated to be a key regulator not only in cell death pathways including apoptosis and necroptosis but also in inflammation and host immune responses. In this study, a RIP3 ortholog named Lc-RIP3 is identified in large yellow [...] Read more.
Receptor-interacting protein 3 (RIP3) has been demonstrated to be a key regulator not only in cell death pathways including apoptosis and necroptosis but also in inflammation and host immune responses. In this study, a RIP3 ortholog named Lc-RIP3 is identified in large yellow croaker (Larimichthys crocea). The open reading frame (ORF) of Lc-RIP3 is 1524 bp long and encodes a protein of 507 amino acids (aa). The deduced Lc-RIP3 protein has an N-terminal kinase domain and a C-terminal RHIM domain, and the genome organization of Lc-RIP3 is conserved in teleosts with 12 exons and 11 introns but is different from that in mammals, which comprises 10 exons and 9 introns. Confocal microscopy revealed that Lc-RIP3 is a cytosolic protein. The expression analysis at the mRNA level indicated that Lc-RIP3 is ubiquitously distributed in various tissues/organs, and could be up-regulated under poly I:C, LPS, PGN, and Pseudomonas plecoglossicida stimulation in vivo. Notably, Lc-RIP3 could induce NF-κB but not IRF3 activation. In addition, Lc-RIP3 co-expression with Lc-TRIF, Lc-MAVS, or Lc-IRF3 significantly abolishes the activation of NF-κB but enhances the induction of IRF3 activity. Moreover, NF-κB activity could be up-regulated when Lc-RIP3 is co-expressed with Lc-RIP1 or Lc-IRF7. These results collectively indicate that Lc-RIP3 acts as an important regulator in host innate immune signaling in teleosts. Full article
(This article belongs to the Special Issue Bacterial Infection and PRRs-Mediated Innate Immune Responses in Fish)
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20 pages, 5575 KiB  
Article
Crosstalks between NOD1 and Histone H2A Contribute to Host Defense against Streptococcus agalactiae Infection in Zebrafish
by Xiaoman Wu, Fan Xiong, Hong Fang, Jie Zhang and Mingxian Chang
Antibiotics 2021, 10(7), 861; https://doi.org/10.3390/antibiotics10070861 - 15 Jul 2021
Cited by 3 | Viewed by 2073
Abstract
Correlation studies about NOD1 and histones have not been reported. In the present study, we report the functional correlation between NOD1 and the histone H2A variant in response to Streptococcus agalactiae infection. In zebrafish, NOD1 deficiency significantly promoted S. agalactiae proliferation and decreased [...] Read more.
Correlation studies about NOD1 and histones have not been reported. In the present study, we report the functional correlation between NOD1 and the histone H2A variant in response to Streptococcus agalactiae infection. In zebrafish, NOD1 deficiency significantly promoted S. agalactiae proliferation and decreased larval survival. Transcriptome analysis revealed that the significantly enriched pathways in NOD1−/− adult zebrafish were mainly involved in immune and metabolism. Among 719 immunity-associated DEGs at 48 hpi, 74 DEGs regulated by NOD1 deficiency were histone variants. Weighted gene co-expression network analysis identified that H2A, H2B, and H3 had significant associations with NOD1 deficiency. Above all, S. agalactiae infection could induce the expression of intracellular histone H2A, as well as NOD1 colocalized with histone H2A, both in the cytoplasm and cell nucleus in the case of S. agalactiae infection. The overexpression of H2A variants such as zfH2A-6 protected against S. agalactiae infection and could improve cell survival in NOD1-deficient cells. Furthermore, NOD1 could interact with zfH2A-6 and cooperate with zfH2A-6 to inhibit the proliferation of S. agalactiae. NOD1 also showed a synergetic effect in inducing the expression of many antibacterial genes, especially antibacterial pattern recognition receptors PGRP2, PGRP5, and PGRP6. Collectively, these results firstly highlight the roles of NOD1 deficiency in the regulation of immune-related and metabolic pathways, and the correlation between zebrafish NOD1 and histone H2A variant in the defense against S. agalactiae infection. Full article
(This article belongs to the Special Issue Bacterial Infection and PRRs-Mediated Innate Immune Responses in Fish)
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16 pages, 3515 KiB  
Article
Hepcidin Protects Yellow Catfish (Pelteobagrus fulvidraco) against Aeromonas veronii-Induced Ascites Disease by Regulating Iron Metabolism
by Manquan Fu, Rui Kuang, Weicheng Wang, Yunzhen Yu, Taoshan Ai, Xiaoling Liu, Jianguo Su and Gailing Yuan
Antibiotics 2021, 10(7), 848; https://doi.org/10.3390/antibiotics10070848 - 12 Jul 2021
Cited by 14 | Viewed by 2661
Abstract
Aeromonas veronii (A. veronii) is one of the main pathogens causing bacterial diseases in aquaculture. Although previous studies have shown that hepcidin as an antimicrobial peptide can promote fish resistance to pathogenic bacterial infections, but the mechanisms remain unclear. Here, we [...] Read more.
Aeromonas veronii (A. veronii) is one of the main pathogens causing bacterial diseases in aquaculture. Although previous studies have shown that hepcidin as an antimicrobial peptide can promote fish resistance to pathogenic bacterial infections, but the mechanisms remain unclear. Here, we expressed and purified recombinant yellow catfish (Pelteobagrus fulvidraco) hepcidin protein (rPfHep). rPfHep can up-regulate the expression of ferritin and enhance the antibacterial activity in primary hepatocytes of yellow catfish. We employed berberine hydrochloride (BBR) and Fursultiamine (FSL) as agonists and antagonists for hepcidin, respectively. The results indicated that agonist BBR can inhibit the proliferation of pathogenic bacteria, and the antagonist FSL shows the opposite effect. After gavage administration, rPfHep and the agonist BBR can enhance the accumulation of iron in liver, which may hinder the iron transport and limit the amount of iron available to pathogenic bacteria. Moreover, rPfHep and the agonist BBR can also reduce the mortality rate, bacterial load and histological lesions in yellow catfish infected with A. veronii. Therefore, hepcidin is an important mediator of iron metabolism, and it can be used as a candidate target for prevent bacterial infections in yellow catfish. Hepcidin and BBR have potential application value in preventing anti-bacterial infection. Full article
(This article belongs to the Special Issue Bacterial Infection and PRRs-Mediated Innate Immune Responses in Fish)
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