ArticleJournal of immunology (Baltimore, Md. : 1950)2012
SHP-1 as a critical regulator of Mycoplasma pneumoniae-induced inflammation in human asthmatic airway epithelial cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.European journal of pediatrics · 2026Review
- The JAK-STAT pathway in allergic diseases: from pathogenesis to targeted therapy.Biomarker research · 2026Review
- A computational-based new treatment strategy with three-armed RCT on Mycoplasma pneumoniae pneumonia in children.Chinese medicine · 2025Article
- CCL20 Expression via AKT-ERK1/2-AP1 Pathway inJournal of inflammation research · 2025Article
- Modulation of IL-4/IL-13 cytokine signaling in the context of allergic disease.The Journal of allergy and clinical immunology · 2022Review
- Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy.Signal transduction and targeted therapy · 2022Review
- Exploration of the Molecular Mechanisms ofBioMed research international · 2022Article
- Novel Strategies for Solubility and Bioavailability Enhancement of Bufadienolides.Molecules (Basel, Switzerland) · 2021Review
- HNRNPH1 Is a Novel Regulator Of Cellular Proliferation and Disease Progression in Chronic Myeloid Leukemia.Frontiers in oncology · 2021Article
- [Effect of annexin A2 on EGFR/NF-κB signal transduction and mucin expression in human airway epithelial cells treated with Mycoplasma pneumoniae].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Article
- Capsular Polysaccharide is a Main Component ofMediators of inflammation · 2017Article
- Protein tyrosine phosphatase SHP-1: resurgence as new drug target for human autoimmune disorders.Immunologic research · 2016Review
- Changes in levels of IL-9, IL-17, IFN-γ, dendritic cell numbers and TLR expression in peripheral blood in asthmatic children with Mycoplasma pneumoniae infection.International journal of clinical and experimental pathology · 2015Article
- Neutrophil dependence of vascular remodeling after Mycoplasma infection of mouse airways.The American journal of pathology · 2014Article
- Macrophage-activating lipopeptide-2 requires Mal and PI3K for efficient induction of heme oxygenase-1.PloS one · 2014Article
- House dust mite allergen Der f 2 induces interleukin-13 expression by activating the PI3K/Akt pathway.Immunologic research · 2013Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Asthma is a chronic inflammatory disease in which airway epithelial cells are the first line of defense against exposure of the airway to infectious agents. Src homology protein (SHP)-1, a protein tyrosine phosphatase, is a negative regulator of signaling pathways that are critical to the development of asthma and host defense. We hypothesize that SHP-1 function is defective in asthma, contributing to the increased inflammatory response induced by Mycoplasma pneumoniae, a pathogen known to exacerbate asthma. M. pneumoniae significantly activated SHP-1 in airway epithelial cells collected from nonasthmatic subjects by bronchoscopy with airway brushing but not in cells from asthmatic subjects. In asthmatic airway epithelial cells, M. pneumoniae induced significant PI3K/Akt phosphorylation, NF-κB activation, and IL-8 production compared with nonasthmatic cells, which were reversed by SHP-1 overexpression. Conversely, SHP-1 knockdown significantly increased IL-8 production and PI3K/Akt and NF-κB activation in the setting of M. pneumoniae infection in nonasthmatic cells, but it did not exacerbate these three parameters already activated in asthmatic cells. Thus, SHP-1 plays a critical role in abrogating M. pneumoniae-induced IL-8 production in nonasthmatic airway epithelial cells through inhibition of PI3K/Akt and NF-κB activity, but it is defective in asthma, resulting in an enhanced inflammatory response to infection.
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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.