Differential Lung Inflammation and Injury with Tobacco Smoke Exposure in Wistar Kyoto and Spontaneously Hypertensive Rats

Details

• Personal Author:
  Pham AK ; Pinkerton KE ; Qiu X ; Smiley-Jewell S ; Upadhyay P ; Uyeminami D ; Wu C-W ; Xu J ; Zhao D
• Description:
  Objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide and has been associated with periods of intense lung inflammation. The objective of this study was to characterize whether similar rat strains, possessing different genetic predispositions, might play a role in exacerbating the pathophysiology of COPD-like cellular and structural changes with progressive 12-week exposure to tobacco smoke (TS). Normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SH) rats were compared. Materials and methods: WKY and SH rats were exposed to filtered air or to tobacco smoke at a particulate concentration of 80 mg/m3 for 4, 8, or 12 weeks. Necropsy was performed 24 h after the last exposure to obtain cells by bronchoalveolar lavage for total cell and differential counts. Scoring of lung tissues and immunohistochemical staining for M1 (pro-inflammatory) and M2 (anti-inflammatory) macrophages were performed on paraffin-embedded lung sections. Results and discussion: With progressive exposure, TS-exposed SH rats demonstrated significant airspace enlargement, mucin production, and lung inflammation compared to their FA control and TS-matched WKY rats. Moreover, SH rats also demonstrated increased expression of the M1 marker in alveolar macrophages compared to FA control, as well as the M2 marker compared to controls and TS-exposed WKY rats. Conclusion: The progressive tobacco smoke exposure contributes to persistent lung injury and inflammation that can be significantly enhanced by rat strain susceptibility in the genesis of COPD. [Description provided by NIOSH]
• Subjects:
  Animals Blood Immune System Lung Macrophages Occupational Health Respiratory System Safety Smoke Tobacco Products Toxicology

  More +
• Keywords:
  Animal Studies Author Keywords: Chronic Obstructive Pulmonary Disease Chronic Obstructive Pulmonary Disease COPD Immunochemistry Inhalation Lung Tissue Macrophage Spontaneously Hypertensive Rats Tobacco Smoke Toxicopathology Wistar Kyoto Rats

  More +
• ISSN:
  0895-8378
• Document Type:
  Text
• Funding:
  Cooperative Agreement
• Genre:
  Journal Article
• Place as Subject:
  California ; OSHA Region 9
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  328-341
• Volume:
  32
• Issue:
  8
• NIOSHTIC Number:
  nn:20068335
• Citation:
  Inhal Toxicol 2020 Jul; 32(8):328-341
• Contact Point Address:
  Kent E. Pinkerton, School of Medicine; Anatomy,Physiology and Cell Biology, School of Veterinary Medicine; Center for Health and the Environment, University of California, Davis, CA 95616, USA
• Email:
  kepinkerton@ucdavis.edu
• Federal Fiscal Year:
  2020
• NORA Priority Area:
  Agriculture, Forestry and Fishing
• Performing Organization:
  University of California - Davis
• Peer Reviewed:
  True
• Start Date:
  20010930
• Source Full Name:
  Inhalation Toxicology
• End Date:
  20270929
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:d5966e9dc394a4302a35b58cf82168392d79aec6d9ed970daa56c333c5d5258a0f4cff792b51be2c09dac64d7f99ba13b17276b6933d73198e6a660c6e04250f
• Download URL:
  https://stacks.cdc.gov/view/cdc/230502/cdc_230502_DS1.pdf
• File Type:
  [PDF - 3.48 MB ]