ArticleAmerican journal of respiratory cell and molecular biology2018
Lung Defense through IL-8 Carries a Cost of Chronic Lung Remodeling and Impaired Function.
Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 67 citations in OpenAlex.
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- Serine/threonine kinase 33 mediates thrombin-induced interleukin-8 release from human lung epithelial cells in severe asthma.Respiratory research · 2025Article
- Inflammatory Phenotypes of Bronchiectasis.Journal of personalized medicine · 2025Review
- Functional characterization of human IL-8 in vascular stenosis using a novel humanized transgenic mouse model.Vascular pharmacology · 2024Article
- Protein kinase D1 in myeloid lineage cells contributes to the accumulation of CXCR3Frontiers in immunology · 2024Article
- Neutrophil Extracellular Traps in Airway Diseases: Pathological Roles and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Liquid application dosing alters the physiology of air-liquid interface (ALI) primary human bronchial epithelial cell/lung fibroblast co-cultures andFrontiers in toxicology · 2023Article
- Exercise Rehabilitation and Chronic Respiratory Diseases: Effects, Mechanisms, and Therapeutic Benefits.International journal of chronic obstructive pulmonary disease · 2023Review
- Club cell protein (CC)16 as potential lung injury marker in a porcine 72 h polytrauma model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Perfluorooctane Sulfonic Acid Disrupts Protective Tight Junction Proteins via Protein Kinase D in Airway Epithelial Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Thrombin induces IL-8/CXCL8 expression by DCLK1-dependent RhoA and YAP activation in human lung epithelial cells.Journal of biomedical science · 2022Article
- Identification of ANXA2 on epithelial cells as a new receptor for secretory IgA using immunoprecipitation and mass spectrometry.Clinical and experimental immunology · 2022Article
- Emerging Glycation-Based Therapeutics-Glyoxalase 1 Inducers and Glyoxalase 1 Inhibitors.International journal of molecular sciences · 2022Review
- Claudin-18 expression under hyperoxia in neonatal lungs of bronchopulmonary dysplasia model rats.Frontiers in pediatrics · 2022Article
- Environmental Exposures and Lung Aging: Molecular Mechanisms and Implications for Improving Respiratory Health.Current environmental health reports · 2021Review
- SSRIs: Applications in inflammatory lung disease and implications for COVID-19.Neuropsychopharmacology reports · 2021Review
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16 authors at 2 institutions in 1 country.
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Abstract
IL-8-dependent inflammation is a hallmark of host lung innate immunity to bacterial pathogens, yet in many human lung diseases, including chronic obstructive pulmonary disease, bronchiectasis, and pulmonary fibrosis, there are progressive, irreversible, pathological changes associated with elevated levels of IL-8 in the lung. To better understand the duality of IL-8-dependent host immunity to bacterial infection and lung pathology, we expressed human IL-8 transgenically in murine bronchial epithelium, and investigated the impact of overexpression on lung bacterial clearance, host immunity, and lung pathology and function. Persistent IL-8 expression in bronchial epithelium resulted in neutrophilia, neutrophil maturation and activation, and chemotaxis. There was enhanced protection against challenge with Pseudomonas aeruginosa, and significant changes in baseline expression of innate and adaptive immunity transcripts for Ccl5, Tlr6, IL-2, and Tlr1. There was increased expression of Tbet and Foxp3 in response to the Pseudomonas antigen OprF, indicating a regulatory T-cell phenotype. However, this enhanced bacterial immunity came at a high price of progressive lung remodeling, with increased inflammation, mucus hypersecretion, and fibrosis. There was increased expression of Ccl3 and reduced expression of Claudin 18 and F11r, with damage to epithelial organization leading to leaky tight junctions, all of which resulted in impaired lung function with reduced compliance, increased resistance, and bronchial hyperreactivity as measured by whole-body plethysmography. These results show that IL-8 overexpression in the bronchial epithelium benefits lung immunity to bacterial infection, but specifically drives lung damage through persistent inflammation, lung remodeling, and damaged tight junctions, leading to impaired lung function.
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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.