ArticlePLoS pathogens2009
CD14 signaling restrains chronic inflammation through induction of p38-MAPK/SOCS-dependent tolerance.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
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- Toll-like receptor 1 polymorphism is associated with impaired immune tolerance, dysregulated inflammatory responses toFrontiers in immunology · 2025Article
- Olanzapine Induces Inflammation and Immune Response via Activating ER Stress in the Rat Prefrontal Cortex.Current medical science · 2021Article
- Sexual Dimorphic Role of CD14 (Cluster of Differentiation 14) in Salt-Sensitive Hypertension and Renal Injury.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Protection againstHuman vaccines & immunotherapeutics · 2020Article
- A joint effort: The interplay between the innate and the adaptive immune system in Lyme arthritis.Immunological reviews · 2020Review
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- Suppressors of Cytokine Signaling (SOCS)1 and SOCS3 Proteins Are Mediators of Interleukin-10 Modulation of Inflammatory Responses Induced byMediators of inflammation · 2020Article
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- Necrotizing enterocolitis is associated with acute brain responses in preterm pigs.Journal of neuroinflammation · 2018Article
- Induction of Interleukin 10 by Borrelia burgdorferi Is Regulated by the Action of CD14-Dependent p38 Mitogen-Activated Protein Kinase and cAMP-Mediated Chromatin Remodeling.Infection and immunity · 2018Article
- Anti-inflammatory roles of p38α MAPK in macrophages are context dependent and require IL-10.Journal of leukocyte biology · 2017Article
- Phagocytic Receptors Activate Syk and Src Signaling during Borrelia burgdorferi Phagocytosis.Infection and immunity · 2017Article
- Infection with the Lyme disease pathogen suppresses innate immunity in mice with diet-induced obesity.Cellular microbiology · 2017Article
- SOCS Proteins as Regulators of Inflammatory Responses Induced by Bacterial Infections: A Review.Frontiers in microbiology · 2017Review
- Lyme borreliosis.Nature reviews. Disease primers · 2016Review
- Plasma levels of eight different mediators and their potential as biomarkers of various clinical malaria conditions in African children.Malaria journal · 2016Article
- Borrelia burgdorferi induces a type I interferon response during early stages of disseminated infection in mice.BMC microbiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Current thinking emphasizes the primacy of CD14 in facilitating recognition of microbes by certain TLRs to initiate pro-inflammatory signaling events and the importance of p38-MAPK in augmenting such responses. Herein, this paradigm is challenged by demonstrating that recognition of live Borrelia burgdorferi not only triggers an inflammatory response in the absence of CD14, but one that is, in part, a consequence of altered PI3K/AKT/p38-MAPK signaling and impaired negative regulation of TLR2. CD14 deficiency results in increased localization of PI3K to lipid rafts, hyperphosphorylation of AKT, and reduced activation of p38. Such aberrant signaling leads to decreased negative regulation by SOCS1, SOCS3, and CIS, thereby compromising the induction of tolerance in macrophages and engendering more severe and persistent inflammatory responses to B. burgdorferi. Importantly, these altered signaling events and the higher cytokine production observed can be mimicked through shRNA and pharmacological inhibition of p38 activity in CD14-expressing macrophages. Perturbation of this CD14/p38-MAPK-dependent immune regulation may underlie development of infectious chronic inflammatory syndromes.
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Registered trials
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.