Characterization of Rabbit Nucleotide-Binding Oligomerization Domain 1 (NOD1) and the Role of NOD1 Signaling Pathway during Bacterial Infection

Guo, Mengjiao; Wu, Fahao; Hao, Guangen; Li, Rong; Li, Ning; Shang, Yue; Wei, Liangmeng; Chai, Tongjie

doi:10.3389/fimmu.2017.01278

Cited by 11 publications

(4 citation statements)

References 56 publications

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“…The synthesized cDNA was stored at − 20 °C. For qRT–PCR, the primers for Tlr2 , Tlr4 , Il1β, Il6 , Il8 , Tnf-α, and Gapdh were based on the previous studies (Table 1 ) [ 19 , 20 ]. qRT–PCR reaction system was carry out in a total volume of 20 μL with TransStart R Tip Green qPCR SuperMix (+Dye II) (Transgen Biotech Co., Ltd.).…”

Section: Methodsmentioning

confidence: 99%

Pathogenicity, colonization, and innate immune response to Pasteurella multocida in rabbits

Yang

Zhang

et al. 2022

BMC Vet Res

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Background Pasteurella multocida (P. multocida) infection can cause a series of diseases in different animals and cause huge economic losses to the breeding industry. P. multocida is considered to be one of the most significant pathogens in rabbits. In order to elucidate the pathogenic mechanism and innate immune response of P. multocida, an infection experiment was carried out in this study. Results Our results showed that the clinical symptoms of rabbits were severe dyspnoea and serous nasal fluid. During the course of the disease, the deaths peaked at 2 days post infection (dpi) and mortality rate was 60%. The pathological changes of the lung, trachea, and thymus were observed. In particular, consolidation and abscesses appeared in lung. Histopathologic changes in rabbits showed edema, hemorrhage, and neutrophil infiltration in the lung. P. multocida can rapidly replicate in a variety of tissues, and the colonization in most of the tested tissues reached the maximum at 2 dpi and then decreased at 3 dpi. The number of P. multocida in lung and thymus remained high level at 3 dpi. Toll-like receptors 2 and 4 signaling pathways were activated after P. multocida infection. The expression of Il1β, Il6, Il8, and Tnf-α was significantly increased. The expression of most proinflammatory cytokines peaked at 2 dpi and decreased at 3 dpi, and the expression trend of cytokines was consistent with the colonization of P. multocida in rabbit tissues. Conclusions The P. multocida can rapidly replicate in various tissues of rabbit and cause bacteremia after infection. TLRs signaling pathways were activated after P. multocida infection, significantly inducing the expression of proinflammatory cytokines, which is might the main cause of respiratory inflammation and septicemia.

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Section: Methodsmentioning

confidence: 99%

Pathogenicity, colonization, and innate immune response to Pasteurella multocida in rabbits

Yang

Zhang

et al. 2022

BMC Vet Res

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“…Phosphorylated CagA interacts with Shp2, a host protein that binds to CagA, this complex dephosphorylates the focal adhesion kinase and in turn activates a signal pathway that involves ERK proteins [52,53]. The transferred peptidoglycan promotes the activation of the pattern-recognition molecule Nod1 within the cytosol of the host cell [54] and subsequently induces the expression of IL-6 and IL-8 as well as MAPK phosphorylation [55][56][57]. The phosphorylation independent activity of CagA disrupts E-cadherin and ZO-1 and consequently cell-to-cell junctions in polarized epithelial cells [10,49,58,59].…”

Section: Cagamentioning

confidence: 99%

Effect of Helicobacter pylori on Tight Junctions in Gastric Epithelia

Rendón-Huerta¹,

García-García²,

Estrada³

2021

Helicobacter Pylori - From First Isolation to 2021

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Molecular complexes grouped under the names of tight, adherent or gap junction regulate the flow of water, ions and macromolecules through epithelium paracellular spaces. The main constituents of tight junctions are claudins, a family of 26 different proteins whose expression and distribution are tissue specific but varies in tumors. A change in claudin 1, 3, 4, 5, 6, 7, 9 and 18 expression, that contributes to lose epithelial cohesion, has been associated to enhanced cell proliferation, migration, and invasiveness in gastric neoplastic tissue. Chronic inflammation process induced by H. pylori infection, a major risk factor for gastric cancer development, disrupts tight junctions via CagA gene, Cag pathogenicity island, and VacA, but the effect upon the epithelial barrier of H. pylori lipopolysaccharides or H. pylori-induced up-regulation of mTOR and ERK signaling pathways by microRNA-100 establishes new concepts of proof.

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“…1C). Previous studies have shown that ectopic overexpression of NOD1 led to the induction of NF-kB signaling and the production of proinflammatory cytokines (36,37). To distinguish NOD1dependent or cytokine-mediated upregulation of antiviral genes, supernatant transfer experiments were performed in the naive ZF4 cells.…”

Section: Nod1 Regulates Antiviral Response and The Expression Of Rlr Pathway Membersmentioning

confidence: 99%

NOD1 Promotes Antiviral Signaling by Binding Viral RNA and Regulating the Interaction of MDA5 and MAVS

Zhang

et al. 2020

The Journal of Immunology

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Nucleotide oligomerization domain-like receptors (NLRs) and RIG-I-like receptors (RLRs) detect diverse pathogen-associated molecular patterns to activate the innate immune response. The role of mammalian NLR NOD1 in sensing bacteria is well established. Although several studies suggest NOD1 also plays a role in sensing viruses, the mechanisms behind this are still largely unknown. In this study, we report on the synergism and antagonism between NOD1 and MDA5 isoforms in teleost. In zebrafish, the overexpression of NOD1 enhances the antiviral response and mRNA abundances of key antiviral genes involved in RLR-mediated signaling, whereas the loss of NOD1 has the opposite effect. Notably, spring viremia of carp virus-infected NOD1 2/2 zebrafish exhibit reduced survival compared with wild-type counterparts. Mechanistically, NOD1 targets MDA5 isoforms and TRAF3 to modulate the formation of MDA5-MAVS and TRAF3-MAVS complexes. The cumulative effects of NOD1 and MDA5a (MDA5 normal form) were observed for the binding with poly(I:C) and the formation of the MDA5a-MAVS complex, which led to increased transcription of type I IFNs and ISGs. However, the antagonism between NOD1 and MDA5b (MDA5 truncated form) was clearly observed during proteasomal degradation of NOD1 by MDA5b. In humans, the interactions between NOD1-MDA5 and NOD1-TRAF3 were confirmed. Furthermore, the roles that NOD1 plays in enhancing the binding of MDA5 to MAVS and poly(I:C) are also evolutionarily conserved across species. Taken together, our findings suggest that mutual regulation between NOD1 and MDA5 isoforms may play a crucial role in the innate immune response and that NOD1 acts as a positive regulator of MDA5/MAVS normal form-mediated immune signaling in vertebrates.

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Characterization of Rabbit Nucleotide-Binding Oligomerization Domain 1 (NOD1) and the Role of NOD1 Signaling Pathway during Bacterial Infection

Cited by 11 publications

References 56 publications

Pathogenicity, colonization, and innate immune response to Pasteurella multocida in rabbits

Pathogenicity, colonization, and innate immune response to Pasteurella multocida in rabbits

Effect of Helicobacter pylori on Tight Junctions in Gastric Epithelia

NOD1 Promotes Antiviral Signaling by Binding Viral RNA and Regulating the Interaction of MDA5 and MAVS

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