The DOI matches its Crossref record; 59 of the 59 references it cites were found in a registry or an index.
Targeted expression of IL-11 in the murine airway causes lymphocytic inflammation, bronchial remodeling, and airways obstruction.
Open accessAbstract
Interleukin-11 is a pleotropic cytokine produced by lung stromal cells in response to respiratory viruses, cytokines, and histamine. To further define its potential effector functions, the Clara cell 10-kD protein promoter was used to express IL-11 and the airways of the resulting transgene mice were characterized. In contrast to transgene (-) littermates, the airways of IL-11 transgene (+) animals manifest nodular peribronchiolar mononuclear cell infiltrates and impressive airways remodeling with subepithelial fibrosis. The inflammatory foci contained large numbers of B220(+) and MHC Class II(+) cells and lesser numbers of CD3(+), CD4(+), and CD8(+) cells. The fibrotic response contained increased amounts of types III and I collagen, increased numbers of alpha smooth muscle actin and desmin-containing cells and a spectrum of stromal elements including fibroblasts, myofibroblasts, and smooth muscle cells. Physiologic evaluation also demonstrated that 2-mo-old transgene (+) mice had increased airways resistance and non-specific airways hyperresponsiveness to methacholine when compared with their transgene (-) littermates. These studies demonstrate that the targeted expression of IL-11 in the mouse airway causes a B and T cell-predominant inflammatory response, airway remodeling with increased types III and I collagen, the local accumulation of fibroblasts, myofibroblasts, and myocytes, and obstructive physiologic dysregulation. IL-11 may play an important role in the inflammatory and fibrotic responses in viral and/or nonviral human airway disorders.
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“global deletion of the bacterial signaling adaptor molecule MyD88 (a critical signaling adaptor molecule for all TLRs, except TLR3155) reduced intestinal fibrosis in a model of Salmonella-induced colitis156”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [156]
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Fibrosis: from mechanisms to medicines
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Self-citationIL-17 is increased in asthmatic airways and induces human bronchial fibroblasts to produce cytokines
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Metadata
- Authors
- Tang, W., Geba, G. P., Zheng, T., Ray, P., Homer, R. J., Kuhn, C., Flavell, R. A., & Elias, J. A.
- Affiliations
- Yale University (US)
- United States Department of Veterans Affairs (US)
- Miriam Hospital (US)
- Brown University (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1996-12-15
- Volume
- 98
- Issue
- 12
- Pages
- 2845-2853
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC507752
- OpenAlex
- W2075223992
- Cited by
- 210
- References
- 59
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 6 · 2022: 3 · 2021: 3 · 2020: 7 · 2019: 9 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 2 · 2013: 2 · 2012: 5
- FWCI
- 6.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl054989-03, 5r01hl036708-12)
- National Heart, Lung, and Blood Institute (HL54989, HL-36708)
- National Institute of Allergy and Infectious Diseases (AI-34593)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- interleukin-11, airway inflammation, airway remodeling, airway obstruction, airway hyperresponsiveness, transgenic mice, lymphocytic inflammation, B cells, T cells, subepithelial fibrosis, collagen deposition, myofibroblasts, smooth muscle cells, fibroblasts, airway resistance, methacholine
- MeSH terms
- Airway Obstruction, Airway Resistance, Animals, Cloning, Molecular, Disease Models, Animal, Gene Expression Regulation, Histocytochemistry, Immunohistochemistry, Lung, Mice, Transgenic, Microscopy, Electron, Promoter Regions, Genetic, Proteins, Pulmonary Fibrosis, Uteroglobin, Blotting, Southern, Blotting, Northern, Methacholine Chloride, Interleukin-11, Mice
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