ArticleAmerican journal of physiology. Lung cellular and molecular physiology2019
MyD88 controls airway epithelial Muc5ac expression during TLR activation conditions from agricultural organic dust exposure.
Article in American journal of physiology. Lung cellular and molecular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Blocking interleukin 33 reduces joint, systemic, and lung inflammatory responses in the combined collagen-induced arthritis-inhalant endotoxin exposure model.The Journal of pharmacology and experimental therapeutics · 2026Article
- The Role of Mucins in Esophageal Inflammatory Diseases.Journal of personalized medicine · 2026Review
- Research progress on the mechanisms of mucus retention after mycoplasma pneumoniae infection.Frontiers in cellular and infection microbiology · 2026Review
- MTOR signaling regulates the development of airway mucous cell metaplasia associated with severe asthma.JCI insight · 2025Article
- Effect of epithelial-specific MyD88 signaling pathway on airway inflammatory response to organic dust exposure.Journal of immunotoxicology · 2023Article
- Mechanistic and Therapeutic Approaches to Occupational Exposure-Associated Allergic and Non-Allergic Asthmatic Disease.Current allergy and asthma reports · 2023Review
- The Mechanism of Lipopolysaccharide's Effect on Secretion of Endometrial Mucins in Female Mice during Pregnancy.International journal of molecular sciences · 2022Article
- Home Dust Mites Promote MUC5AC Hyper-Expression by Modulating the sNASP/TRAF6 Axis in the Airway Epithelium.International journal of molecular sciences · 2022Article
- A porous cervical mucus plug leads to preterm birth induced by experimental vaginal infection in mice.iScience · 2022Article
- The Fim and FhaB adhesins play a crucial role in nasal cavity infection and Bordetella pertussis transmission in a novel mouse catarrhal infection model.PLoS pathogens · 2022Article
- Autophagy of mucin granules contributes to resolution of airway mucous metaplasia.Scientific reports · 2021Article
- Harnessing the Antiinflammatory Power of MyD88 to Reduce Allergic Fungal Inflammation?American journal of respiratory cell and molecular biology · 2021Article
- MyD88 regulates a prolonged adaptation response to environmental dust exposure-induced lung disease.Respiratory research · 2020Article
- Ovalbumin-sensitized mice have altered airway inflammation to agriculture organic dust.Respiratory research · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation from airborne microbes can overwhelm compensatory mucociliary clearance mechanisms, leading to mucous cell metaplasia. Toll-like receptor (TLR) activation via myeloid differentiation factor 88 (MyD88) signaling is central to pathogen responses. We have previously shown that agricultural organic dust extract (ODE), with abundant microbial component diversity, activates TLR-induced airway inflammation. With the use of an established model, C57BL/6J wild-type (WT) and global MyD88 knockout (KO) mice were treated with intranasal inhalation of ODE or saline, daily for 1 wk. ODE primarily increased mucin (Muc)5ac levels relative to Muc5b. Compared with ODE-challenged WT mice, ODE-challenged, MyD88-deficient mice demonstrated significantly increased Muc5ac immunostaining, protein levels by immunoblot, and expression by quantitative PCR. The enhanced Muc5ac levels in MyD88-deficient mice were not explained by differences in the differentiation program of airway secretory cells in naïve mice. Increased Muc5ac levels in MyD88-deficient mice were also not explained by augmented inflammation, IL-17A, or neutrophil elastase levels. Furthermore, the enhanced airway mucins in the MyD88-deficient mice were not due to defective secretion, as the mucin secretory capacity of MyD88-KO mice remained intact. Finally, ODE-induced Muc5ac levels were enhanced in MyD88-deficient airway epithelial cells in vitro. In conclusion, MyD88 deficiency enhances airway mucous cell metaplasia under environments with high TLR activation.
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