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Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
Functional characterization of NLRX1 in rabbit during enterohemorrhagic Escherichia coli infection
Mengjiao Guo1, Congyue Zhang1, Chengcheng Zhang1
1Jiangsu Co-Innovation Center for Prevention of Animal Infectious Diseases and Zoonoses, College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.
Abstract:
Nucleotide oligomerization domain (NOD) like receptor X1 (NLRX1) is a member of pattern recognition receptor, which has been linked to viral response, cancer, and inflammatory diseases. In this study, rabbit NLRX1 (rNLRX1) was firstly cloned from RK-13 cells, which protein contained a NACHT domain and seven LRRs. rNLRX1 was widely expressed in tissues of rabbits, and highly increased in liver, spleen, kidney, and colon after infected with enterohemorrhagic Escherichia coli (EHEC). Overexpression of rNLRX1 negatively regulated NF-κB signaling, and impaired the expression of pro-inflammatory cytokines and defensins. Moreover, deficient of rNLRX1 in RK-13 cells was performed to investigate the possible roles of rNLRX1. Upon EHEC stimulation, knockdown of rNLRX1 markedly enhanced NF-κB activation and downstream responsive cytokines (IL1β and TNFα) and β-defensins (DEFB114, DEFB124, and DEFB125). Furthermore, overexpression of rNLRX1 promoted the proliferation of EHEC, whereas knockdown of rNLRX1 inhibited its growth. Our study identified that rNLRX1 acts as a negative regulatory in anti-microbial responses after EHEC infection.
Insights
Rabbit Nucleotide oligomerization domain (NOD) like receptor X1 (NLRX1) negatively regulates antimicrobial responses. This study found rNLRX1 impairs pro-inflammatory cytokines and defensins, hindering E. coli growth.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Nucleotide oligomerization domain (NOD) like receptor X1 (NLRX1) is a pattern recognition receptor involved in immune responses.
- NLRX1 has been implicated in viral responses, cancer, and inflammatory diseases.
Purpose of the Study:
- To clone and characterize rabbit NLRX1 (rNLRX1).
- To investigate the role of rNLRX1 in enterohemorrhagic Escherichia coli (EHEC) infection and innate immunity.
Main Methods:
- Cloning of rNLRX1 from RK-13 cells.
- Analysis of rNLRX1 expression in rabbit tissues after EHEC infection.
- Overexpression and knockdown studies of rNLRX1 in RK-13 cells.
- Assessment of NF-κB signaling pathway activation, cytokine and defensin expression, and bacterial growth.
Main Results:
- rNLRX1 was cloned and found to be widely expressed in rabbit tissues, with increased levels in liver, spleen, kidney, and colon post-EHEC infection.
- Overexpression of rNLRX1 suppressed NF-κB signaling, pro-inflammatory cytokines, and defensins.
- Knockdown of rNLRX1 enhanced NF-κB activation, cytokine (IL1β, TNFα), and defensin (DEFB114, DEFB124, DEFB125) expression upon EHEC stimulation.
- rNLRX1 overexpression promoted EHEC proliferation, while its knockdown inhibited bacterial growth.
Conclusions:
- rNLRX1 functions as a negative regulator in antimicrobial responses against EHEC infection.
- rNLRX1 plays a crucial role in modulating the host's innate immune response to bacterial pathogens.
