ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Chronic hypersensitivity pneumonitis caused by Saccharopolyspora rectivirgula is not associated with a switch to a Th2 response.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Ex Vivo Overactivation of Lymphocyte Subsets in Fibrotic Hypersensitivity Pneumonitis Is Blunted by a Sphingosine-1-Phosphate Receptor Ligand.International journal of molecular sciences · 2025Article
- Mir-155-5p targets TP53INP1 to promote proliferative phenotype in hypersensitivity pneumonitis lung fibroblasts.Non-coding RNA research · 2024Article
- Increased ER Stress and Unfolded Protein Response Activation in Epithelial and Inflammatory Cells in Hypersensitivity Pneumonitis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- Protein kinase D1 in myeloid lineage cells contributes to the accumulation of CXCR3Frontiers in immunology · 2024Article
- Parallel origins and functions of T cells and ILCs.Clinical and experimental immunology · 2023Review
- 5-methyladenosine regulators play a crucial role in development of chronic hypersensitivity pneumonitis and idiopathic pulmonary fibrosis.Scientific reports · 2023Article
- Muc5b plays a role in the development of inflammation and fibrosis in hypersensitivity pneumonitis induced byAmerican journal of physiology. Lung cellular and molecular physiology · 2022Article
- Novel acute hypersensitivity pneumonitis model induced by airway mycosis and high dose lipopolysaccharide.Respiratory research · 2021Article
- Chronic Occupational Mold Exposure Drives Expansion ofJournal of fungi (Basel, Switzerland) · 2021Article
- Genetic variability of T cell responses in hypersensitivity pneumonitis identified using the BXD genetic reference panel.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- IL-17 in the lung: the good, the bad, and the ugly.American journal of physiology. Lung cellular and molecular physiology · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Hypersensitivity pneumonitis (HP) is an immune-mediated interstitial lung disease that develops following repeated exposure to inhaled environmental antigens. The disease results in alveolitis and granuloma formation and may progress to a chronic form associated with fibrosis; a greater understanding of the immunopathogenic mechanisms leading to chronic HP is needed. We used the Saccharopolyspora rectivirgula (SR) mouse model of HP to determine the extent to which a switch to a Th2-type immune response is associated with chronic HP. Exposure of wild-type (WT) and tlr2/9(-/-) mice to SR for 14 wk resulted in neutrophilic and lymphocytic alveolitis that was not dependent on Toll-like receptors (TLRs) 2 and 9. Long-term exposure of WT mice to SR resulted in a significant increase in collagen deposition, protein leakage, and IL-1α accompanied by a decrease in quasistatic compliance and total lung capacity compared with unexposed mice. This was associated with an increase in IL-17 but not IL-4 production or recruitment of Th2 cells. tlr2/9(-/-) mice exhibited an increase in protein leakage but less IL-1α and collagen deposition in the lungs compared with WT mice, yet they still displayed a decrease in quasistatic compliance, although total lung capacity was not affected. These mice exhibited an increase in both IL-13 and IL-17, which suggests that IL-13 may ameliorate some of the lung damage caused by long-term SR exposure. Our results suggest that lung pathology following long-term SR exposure in WT mice is associated with the IL-17 response and that TLRs 2 and 9 may inhibit the development of the IL-13/Th2 response.
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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.