TRAF3 enhances TRIF-mediated signaling via NF-κB and IRF3 activation in large yellow croaker Larimichthys crocea

Zou, Peng; Shen, Juan Juan; Liu, Ying; Zhang, Ziping; Wang, Yi Lei

doi:10.1016/j.fsi.2019.12.024

Cited by 23 publications

(19 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An expression pattern analysis showed that Lc-RIP3 was constitutively expressed in all the examined organs/tissues in healthy large yellow croakers with the highest expression in the gill, which was consistent with our data that Lc-RIP1 was highly expressed in the gill (unpublished results). In addition, many immune-related genes such as TRIF, TRAF3, IL-17, and TLR21 were also found to exhibit the highest expression level in the gill of large yellow croakers [20,[24][25][26], implying the important function of the gill-associated lymphoid tissue (GIALT) in the mucosa immunity of teleosts [27]. In addition, the expression patterns of Lc-RIP3 in the gill, intestine, spleen, head kidney, blood, and trunk kidney were significantly up-regulated in response to poly I:C, LPS, PGN, and P. plecoglossicida stimulation, which were consistent with studies of other teleosts that RIP3 in half-smooth tongue sole could be induced under Vibrio anguillarum or poly I:C treatment [15] and black carp RIP3 could also be activated in response to poly I:C or LPS stimulation [16], suggesting the possible roles of RIP3 in both bacterial and viral-induced immune responses in teleosts.…”

Section: Discussionmentioning

confidence: 99%

“…They were maintained in laboratory recirculating seawater systems. After acclimating for two weeks, the healthy fish were used for the subsequent experiments as per our previous reports [20,24].…”

Section: Fish Cell Lines and Transfectionmentioning

confidence: 99%

“…To examine the expression patterns of RIP3 under various immune stimulations, five groups of healthy fish were injected with different PAMPs and bacteria as described previously [20,24]. The control group of fish was injected intraperitoneally with 100 μL PBS.…”

Section: Immune Stimulation and Qrt-pcrmentioning

confidence: 99%

“…After staining with DAPI, the cells were visualized and imaged using a confocal microscope (Leica TCS SP8, Germany). The cells were subsequently collected and lysed in a RIPA buffer (Beyotime, Shanghai, China) containing protease inhibitors (Beyotime, Shanghai, China) for the detection of RIP3-GFP and the pTurboGFP fusion proteins using a Western blotting analysis as per our previous reports [20,24] with the primary antibody (Anti-TurboGFP antibody, Evrogen, CAT. #AB513) diluted at 1:5000.…”

Section: Confocal Microscopymentioning

confidence: 99%

See 3 more Smart Citations

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

Zou

Liu

et al. 2021

Antibiotics

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Fish Cell Lines and Transfectionmentioning

confidence: 99%

Section: Immune Stimulation and Qrt-pcrmentioning

confidence: 99%

Section: Confocal Microscopymentioning

confidence: 99%

See 2 more Smart Citations

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

Zou

Liu

et al. 2021

Antibiotics

Self Cite

View full text Add to dashboard Cite

show abstract

“…During PAMPs recognition in the endosome, TLR3 interacts TRIFdependently with TRIF. Zebrafish TRIF recruit two typical downstream factors RIP1 and TBK1 [17] [42] to activate NF-κB and activate IFN-β in an IRF3/7 independent manner [34] , and large yellow croaker traf 3 enhances TRIF-dependent pathway via NF-κB and IRF3 activation [43] . And then, leading the expression of TRIF and induce the activation of downstream signaling pathways.…”

Section: Trif-dependent Pathway In Teleostmentioning

confidence: 99%

Adaptor Molecule TRIF in Teleost

Wang¹,

Hu²

2020

JCMR

View full text Add to dashboard Cite

The immune defense mechanism mainly depends on the recognition and response of innate immune signaling receptors PRRs to PAMPs or DAMPs. TLRs family is an important category in PRRs, stimulatory cytokines and interferon type I (IFN) are produced through TRIF-or MyD88-dependent after TLRs recognition PAMPs or DAMPs, which regulate innate and adaptive immunity responses. TLR3 only relies on the TRIF-dependent pathway for downstream signaling, TLR4 can conduct downstream signaling through both TRIF- and MyD88-dependent pathways. Teleosts TLR3 detects viral and additionally bacterial PAMPs, while TLR3-mediated activation of mammalian immune responses only depends on viral double-stranded RNA intermediates. Teleost TLR4 is suggested to down-regulate TLR signaling and/or to interact with alternative receptors such as b2-integrins, whereas mammalian TLR4 associates with CD14 and MD2 in order to sense LPS. In this review, we will further study the structure of TRIF, the TRIF-dependent signaling pathway, and its function in fish, with emphasis on the TRIF-dependent signaling pathway and different biological activities. The study of TRIF and its role in innate immunity has potential significance for the prevention and treatment of fish diseases.

show abstract

Inhibitory Effects and Related Molecular Mechanisms of Huanglian-Ganjiang Combination Against H1N1 Influenza Virus

Sun

Yan

et al. 2023

Rev. Bras. Farmacogn.

View full text Add to dashboard Cite

Influenza is an infectious acute respiratory disease with complications and a high mortality rate; the effective medicines for influenza therapy are limited. "Huanglian" or Coptidis Rhizoma, Coptis chinensis Franch., Ranunculaceae, and "ganjiang" or Zingiberis Rhizoma, Zingiber officinale Roscoe, Zingiberaceae, combination is clinically used for treating respiratory diseases. HPLC was applied for the quantification of berberine hydrochloride (1.101 mg/ml) and 6-gingerol (38.41 μg/ml) in the H 2 O-soluble extract of the herbal formulation. In this study, the effect of "huanglian"-"ganjiang" extract on influenza virus H1N1-induced acute pulmonary inflammation was evaluated, in addition to the investigation of its anti-influenza mechanism in a mouse model. The analyzed herbal combination inhibited the expression of cytokine IL-6 and stimulated the expression of IL-2 in the serum of influenza virus-infected mice. Meanwhile, the herbal combination downregulated the gene and protein expression levels of TLR3, TLR7, MyD88, RIG-I, MAVS, TRAF3, and NF-κB p65, which are key targets of toll-like and RIG-I-like receptor signaling pathways in mice. In addition, the herbal combination could also promote the combination of intracellular autophagosomes and lysosomes in autophagosome-lysosome formation and improve impaired fusion of autophagosomes and lysosomes by influenza virus. This study suggested that the "huanglian"-"ganjiang" extract may be a candidate therapeutic strategy for the treatment of H1N1 influenza.

show abstract

TRAF3 enhances TRIF-mediated signaling via NF-κB and IRF3 activation in large yellow croaker Larimichthys crocea

Cited by 23 publications

References 46 publications

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

RIP3 Associates with RIP1, TRIF, MAVS, and Also IRF3/7 in Host Innate Immune Signaling in Large Yellow Croaker Larimichthys crocea

Adaptor Molecule TRIF in Teleost

Inhibitory Effects and Related Molecular Mechanisms of Huanglian-Ganjiang Combination Against H1N1 Influenza Virus

Contact Info

Product

Resources

About