ArticleThe Journal of allergy and clinical immunology2012
Mast cell TNF receptors regulate responses to Mycoplasma pneumoniae in surfactant protein A (SP-A)-/- mice.
Article in The Journal of allergy and clinical immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Innate and adaptive immunity pathways linking Mycoplasma pneumoniae to pediatric asthma phenotypes.European journal of pediatrics · 2026Review
- The SP-MrgprX2 Axis in Allergic Rhinitis: a Neuro-immune Paradigm Beyond IgE-mediated Inflammation.Clinical reviews in allergy & immunology · 2026Review
- A computational-based new treatment strategy with three-armed RCT on Mycoplasma pneumoniae pneumonia in children.Chinese medicine · 2025Article
- The Immune Modulatory Role of Surfactants inJournal of inflammation research · 2025Review
- CC16 Deficiency in the Context of Early-LifeInfection and immunity · 2022Article
- Surfactant Protein-A Function: Knowledge Gained From SP-A Knockout Mice.Frontiers in pediatrics · 2021Review
- A 20-Mer Peptide Derived from the Lectin Domain ofInfection and immunity · 2020Article
- TNF Production in Activated RBL-2H3 Cells Requires Munc13-4.Inflammation · 2020Article
- High co-expression of TNF-α and CARDS toxin is a good predictor for refractory Mycoplasma pneumoniae pneumonia.Molecular medicine (Cambridge, Mass.) · 2019Article
- High expression of HMGB1 in children with refractory Mycoplasma pneumoniae pneumonia.BMC infectious diseases · 2018Article
- Hyperoxia treatment of TREK-1/TREK-2/TRAAK-deficient mice is associated with a reduction in surfactant proteins.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Correction notice for TNF-R on mast cells regulate airway responses to Mycoplasma pneumoniae.The Journal of allergy and clinical immunology · 2016Article
- Key mediators in the immunopathogenesis of allergic asthma.International immunopharmacology · 2014Review
Corrections and comments
- Correction · 2015-11-20Error by Third Party · Error in Data · Falsification/Fabrication of Data · Investigation by Company/Institution · Legal Reasons and/or Threats · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · Results Not Reproducible · Unreliable Data · Unreliable Results and/or Conclusions · · EN Potts-Kant named for misconduct; EN Potts-Kant aka EN Potts;
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMycoplasma pneumoniae (Mp) frequently colonizes the airways of patients with chronic asthma and likely contributes to asthma exacerbations. We previously reported that mice lacking surfactant protein A (SP-A) have increased airway hyperresponsiveness (AHR) during M pneumoniae infection versus wild-type mice mediated by TNF-α. Mast cells (MCs) have been implicated in AHR in asthma models and produce and respond to TNF-α.
objectiveDetermine the contribution of MC/TNF interactions to AHR in airways lacking functional SP-A during Mp infection.
methodsBronchoalveolar lavage fluid was collected from healthy and asthmatic subjects to examine TNF-α levels and M pneumoniae positivity. To determine how SP-A interactions with MCs regulate airway homeostasis, we generated mice lacking both SP-A and MCs (SP-A(-/-)Kit(W-sh/W-sh)) and infected them with M pneumoniae.
resultsOur findings indicate that high TNF-α levels correlate with M pneumoniae positivity in human asthmatic patients and that human SP-A inhibits M pneumoniae-stimulated transcription and release of TNF-α by MCs, implicating a protective role for SP-A. MC numbers increase in M pneumoniae-infected lungs, and airway reactivity is dramatically attenuated when MCs are absent. Using SP-A(-/-)Kit(W-sh/W-sh) mice engrafted with TNF-α(-/-) or TNF receptor (TNF-R)(-/-) MCs, we found that TNF-α activation of MCs through the TNF-R, but not MC-derived TNF-α, leads to augmented AHR during M pneumoniae infection when SP-A is absent. Additionally, M pneumoniae-infected SP-A(-/-)Kit(W-sh/W-sh) mice engrafted with TNF-α(-/-) or TNF-R(-/-) MCs have decreased mucus production compared with that seen in mice engrafted with wild-type MCs, whereas burden was unaffected.
conclusionOur data highlight a previously unappreciated but vital role for MCs as secondary responders to TNF-α during the host response to pathogen infection.
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