The Rheumatologist
COVID-19 NewsACR Convergence
  • Connect with us:
  • Facebook
  • Twitter
  • LinkedIn
  • YouTube
  • Feed
  • Home
  • Conditions
    • Rheumatoid Arthritis
    • SLE (Lupus)
    • Crystal Arthritis
      • Gout Resource Center
    • Spondyloarthritis
    • Osteoarthritis
    • Soft Tissue Pain
    • Scleroderma
    • Vasculitis
    • Systemic Inflammatory Syndromes
    • Guidelines
  • Resource Centers
    • Axial Spondyloarthritis Resource Center
    • Gout Resource Center
    • Psoriatic Arthritis Resource Center
    • Rheumatoid Arthritis Resource Center
    • Systemic Lupus Erythematosus Resource Center
  • Drug Updates
    • Biologics & Biosimilars
    • DMARDs & Immunosuppressives
    • Topical Drugs
    • Analgesics
    • Safety
    • Pharma Co. News
  • Professional Topics
    • Ethics
    • Legal
    • Legislation & Advocacy
    • Career Development
      • Certification
      • Education & Training
    • Awards
    • Profiles
    • President’s Perspective
    • Rheuminations
    • Interprofessional Perspective
  • Practice Management
    • Billing/Coding
    • Quality Assurance/Improvement
    • Workforce
    • Facility
    • Patient Perspective
    • Electronic Health Records
    • Apps
    • Information Technology
    • From the College
    • Multimedia
      • Audio
      • Video
  • Resources
    • Issue Archives
    • ACR Convergence
      • Gout Resource Center
      • Axial Spondyloarthritis Resource Center
      • Psoriatic Arthritis
      • Abstracts
      • Meeting Reports
      • ACR Convergence Home
    • American College of Rheumatology
    • ACR ExamRheum
    • Research Reviews
    • ACR Journals
      • Arthritis & Rheumatology
      • Arthritis Care & Research
      • ACR Open Rheumatology
    • Rheumatology Image Library
    • Treatment Guidelines
    • Rheumatology Research Foundation
    • Events
  • About Us
    • Mission/Vision
    • Meet the Authors
    • Meet the Editors
    • Contribute to The Rheumatologist
    • Subscription
    • Contact
  • Advertise
  • Search
You are here: Home / Articles / Interleukin 1-alpha Is Critical for Establishment of Inflammatory Lung Disease

Interleukin 1-alpha Is Critical for Establishment of Inflammatory Lung Disease

January 21, 2014 • By Lara C. Pullen, PhD

  • Tweet
  • Email
Print-Friendly Version / Save PDF

Chronic lung disease is characterized by repeated cycles of injury. The repetitive damage to the airway or alveolar epithelium is a common feature of idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease (COPD), asthma, and bronchiolitis obliterans syndrome (BOS). Not only is epithelial injury common in chronic inflammatory lung diseases, but both alloimmune and nonalloimmune insults to the airway epithelium are associated with an increased incidence of BOS after lung transplantation.

You Might Also Like
  • Anti-Interleukin-6 Therapy for Erdheim-Chester Disease Warrants Study
  • Recent Study Evaluates Nuclear Imaging in Interstitial Lung Disease
  • 2015 ACR/ARHP Annual Meeting: Macrophage Polarization and Its Role in Inflammatory Disease
Also By This Author
  • When Switching Patients to Biosimilars, Communication & Expert Nurses Reduce the Nocebo Effect

Previous studies have suggested that fibroblasts from chronically inflamed tissues show alteration in inflammatory gene expression when compared to fibroblasts from normal tissues. Monika Suwara, a graduate student in Newcastle University in the United Kingdom, and colleagues address the role of fibroblasts in chronic lung disease in a study published in Mucosal Immunology.1

ad goes here:advert-1
ADVERTISEMENT
SCROLL TO CONTINUE

The investigators describe an interleukin (IL) 1α and double-stranded RNA signaling network that triggers a powerful proinflammatory phenotype in lung fibroblasts. The resulting activated fibroblasts have a pattern recognition receptor expression profile that is distinct from that produced by alveolar macrophages.

The team performed their initial experiments using human bronchial epithelial cells that were pulsed with either thapsigargin to induce endoplasmic reticulum (ER) stress or H2O2 to induce oxidative stress. The stressed cells released a damage-associated molecular pattern that was dominated by IL-1α.

ad goes here:advert-2
ADVERTISEMENT
SCROLL TO CONTINUE

Based upon these data, the investigators hypothesized that IL-1α/IL-1 receptor signaling was required for the stimulation of an inflammatory fibroblast phenotype. To test the hypothesis, they treated primary human lung fibroblasts (PHLF) with increasing doses of IL-1α and analyzed the conditioned media from the cells for the presence IL-8. They found that treatment with IL-1α significantly increased the release of IL-8 from PHLFs.

The investigators then used polycytidylic acid as a surrogate for viral RNA. PHLFs had a moderate response to polycytidylic acid. A combined treatment with poly polycytidylic acid and IL-1α resulted in even greater IL-6 and IL-8 gene expression and protein production by the fibroblasts. The investigators then examined transgenic mice that lacked either the IL-1 receptor or IL-1α and treated them with bleomycin. Bleomycin induces significant levels of oxidative stress in lung epithelial cells of normal mice. They found that the transgenic mice had reduced bronchoalveolar lavage (BAL) neutrophilia and collagen deposition in response to bleomycin treatment.

“The bottom line is that sterile airway epithelial injury causes release of IL-1α, which acts as an alarmin to cause lung fibroblasts to develop a potent proinflammatory phenotype. Our in-vivo model suggests that IL-1α plays an important role in driving the neutrophilic inflammatory response to a sterile insult to the lung and its absence ameliorates the neutrophilia and subsequent fibrogenesis. This raises the possibility that IL-1α may be a target to limit chronic lung inflammation and fibrogenesis,” wrote senior author Andrew J. Fisher BMedSci, PhD, also of Newcastle University, to The Rheumatologist.

ad goes here:advert-3
ADVERTISEMENT
SCROLL TO CONTINUE

Pages: 1 2 | Single Page

Filed Under: Research Reviews Tagged With: Chronic lung disease, COPD, fibroblasts, inflammatory lung disease, Interleukin, pulmonary fibrosis

You Might Also Like:
  • Anti-Interleukin-6 Therapy for Erdheim-Chester Disease Warrants Study
  • Recent Study Evaluates Nuclear Imaging in Interstitial Lung Disease
  • 2015 ACR/ARHP Annual Meeting: Macrophage Polarization and Its Role in Inflammatory Disease
  • COPA Genetic Mutation Identified in Lung Disease, Arthritis

Simple Tasks

Learn more about the ACR’s public awareness campaign and how you can get involved. Help increase visibility of rheumatic diseases and decrease the number of people left untreated.

Visit the Simple Tasks site »

Rheumatology Research Foundation

The Foundation is the largest private funding source for rheumatology research and training in the U.S.

Learn more »

American College of Rheumatology

Visit the official website for the American College of Rheumatology.

Visit the ACR »

The Rheumatologist newsmagazine reports on issues and trends in the management and treatment of rheumatic diseases. The Rheumatologist reaches 11,500 rheumatologists, internists, orthopedic surgeons, nurse practitioners, physician assistants, nurses, and other healthcare professionals who practice, research, or teach in the field of rheumatology.

About Us / Contact Us / Advertise / Privacy Policy / Terms of Use / Cookie Preferences

  • Connect with us:
  • Facebook
  • Twitter
  • LinkedIn
  • YouTube
  • Feed

Copyright © 2006–2023 American College of Rheumatology. All rights reserved.

ISSN 1931-3268 (print)
ISSN 1931-3209 (online)