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IL-17A Is Elevated in End-Stage Chronic Obstructive Pulmonary Disease and Contributes to Cigarette Smoke-induced Lymphoid Neogenesis.
IL-17A in the peripheral lung of patients with severe to very severe COPD may contribute to disease progression and development of lymphoid follicles via activation of CXCL12.
IL-17A and the Promotion of Neutrophilia in Acute Exacerbation of Chronic Obstructive Pulmonary Disease.
Functionally, IL-1R1-dependent IL-17A is required for NTHi-exacerbated pulmonary neutrophilia induced by cigarette smoke and may be beneficial to reduce neutrophil recruitment to the airways in patients with COPD.
Chronic Respiratory Aeroallergen Exposure in Mice Induces Epithelial-Mesenchymal Transition in the Large Airways
The results show the contribution of EMT to airway remodeling in chronic asthma-like inflammation and suggest that Th2-polarized airway inflammation can trigger invasion of epithelial cells into the subepithelial regions of the airway wall where they contribute to fibrosis, demonstrating a previously unknown plasticity of theAirway epithelium in allergic airway disease.
Cigarette Smoke Primes the Pulmonary Environment to IL-1α/CXCR-2–Dependent Nontypeable Haemophilus influenzae–Exacerbated Neutrophilia in Mice
A novel mechanism of cigarette smoke priming the lung mucosa toward greater IL-1–driven neutrophilic responses to bacteria, with a central role for the alveolar macrophage in this process is characterized.
Airway epithelial cell differentiation during lung organogenesis requires C/EBPα and C/EBPβ
It is demonstrated that C/EBPα and C/ EBPβ play pivotal, and partly overlapping roles in determining airway epithelial differentiation, with possible implications for tissue regeneration in lung homeostasis and disease.
Lung epithelial CCAAT/enhancer-binding protein-β is necessary for the integrity of inflammatory responses to cigarette smoke.
  • L. Didon, J. Barton, M. Nord
  • Medicine, Biology
    American journal of respiratory and critical care…
  • 15 July 2011
The data suggest a previously unknown role for C/EBPβ and the airway epithelium in mediating inflammatory and innate immune responses to cigarette smoke.
The emerging role of C/EBPs in glucocorticoid signaling: lessons from the lung.
The different mechanisms of GC action as well as the function of the lung-enriched members of the C/EBP transcription factor family are discussed, with emphasis on pulmonary effects, and their potential role in mediating GC resistance is summarized.
Connective tissue growth factor expression pattern in lung development
This is the first report of CTGF expression pattern during lung development, and of an impaired expression in CDH lungs after nitrofen, which is suggested to enhance alveologenesis and microvascular development at late stages of lung development.
Small airway epithelial-C/EBPβ is increased in patients with advanced COPD
C/EBPβ was significantly elevated in advanced COPD vs. asymptomatic smokers, and the expression correlated to lung function decline, an indication of a breakdown of regulatory mechanisms and excessive inflammation.
Elevated Exhaled Nitric Oxide in Allergen-Provoked Asthma Is Associated with Airway Epithelial iNOS
Higher fractional exhaled nitric oxide concentration among asthmatics is associated with elevated iNOS mRNA in the bronchial epithelium, and thus provide a mechanistic explanation for elevated fractions exhaled in allergen-provoked asthma.