ArticleInfection and immunity2008
The cytosolic pattern recognition receptor NOD1 induces inflammatory interleukin-8 during Chlamydia trachomatis infection.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 87 citations in OpenAlex.
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- Mast cells selectively produce inflammatory mediators and impact the early response toFrontiers in immunology · 2023Article
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- Transcriptome Analyses of Chicken Primary Macrophages Infected With AttenuatedFrontiers in microbiology · 2022Article
- Potential IFNγ Modulation of Inflammasome Pathway inLife (Basel, Switzerland) · 2021Article
- Persistence Alters the Interaction between Chlamydia trachomatis and Its Host Cell.Infection and immunity · 2021Article
- An endometrial organoid model of interactions betweenJournal of cell science · 2021Article
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- Apoptosis Functions in Defense against Infection of Mammalian Cells with Environmental Chlamydiae.Infection and immunity · 2020Article
- Modeling MyD88 DeficiencyFrontiers in immunology · 2020Article
- Chlamydial Infection From Outside to Inside.Frontiers in microbiology · 2019Review
- Reticuloendotheliosis Virus Inhibits the Immune Response Acting on Lymphocytes from Peripheral Blood of Chicken.Frontiers in physiology · 2018Article
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- Glycemic Status and Infection Risk in Nondiabetic Autologous Hematopoietic Cell Transplantation Recipients.Biological research for nursing · 2016Article
- A Zebrafish Model forFrontiers in microbiology · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Inflammation is a hallmark of chlamydial infections, but how inflammatory cytokines are induced is not well understood. Pattern recognition receptors (PRR) of the host innate immune system recognize pathogen molecules and activate intracellular signaling pathways that modulate immune responses. The role of PRR such as Toll-like receptors (TLR) and nucleotide-binding oligomerization domain (NOD) proteins in the endogenous interleukin-8 (IL-8) response induced during Chlamydia trachomatis infection is not known. We hypothesized that a PRR is essential for the IL-8 response induced by C. trachomatis infection. RNA interference was used to knock down the TLR signaling partner MyD88 as well as NOD1 and its signaling molecule receptor-interacting protein 2 (RIP2). IL-8 induced at 30 h postinfection by C. trachomatis was dependent on NOD1 signaling through RIP2; however, the IL-8 response was independent of MyD88-dependent TLR signaling. Activation of the extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase cellular signaling pathway, which is essential for up-regulation of IL-8 in response to C. trachomatis infection, was independent of NOD1 or RIP2. We conclude that the endogenous IL-8 response induced by C. trachomatis infection is dependent upon NOD1 PRR signaling through RIP2 as part of a signal system requiring multiple inputs for optimal IL-8 induction. Since ERK is not activated through this pathway, a concomitant interaction between the host and bacteria is additionally required for full activation of the endogenous IL-8 response.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.