High-fat western diet consumption exacerbates silica-induced pulmonary inflammation and fibrosis-dataset

Introduction

Adipose tissue (AT), an endocrine organ, plays a central role in maintenance of whole-body energy homeostasis through its release of adipokines. Obesity, affecting over 40% of American adults, disrupts adipocyte metabolism leading to chronic systemic inflammation and metabolic dysfunction (MetDys). MetDys is associated with impaired lung function, pulmonary hypertension, and asthma. The aim of this study was to investigate the effects of high-fat Western diet (HFWD)-consumption on silica-induced pulmonary inflammation and fibrosis in the F344 rat.

Data Collection Methods

This laboratory-based investigation studied the effects of HFWD-consumption on silica-induced pulmonary inflammation and fibrosis in the F344 rat.

• Six wk old male rats were fed a HFWD or standard (STD; control) for 16 wk prior to inhalation exposure to respirable crystalline silica dust (6 h /d, 5 d / wk, 39 d) with end point measurements taken at 0, 4 and 8 wk post-exposure to silica.
• Animals were maintained on their assigned diet for the duration of the study.
• Endpoint measurements include bronchoalveolar lavage and removal of tissues from euthanized animals. Endpoint measurements include:
  • BAL cell counts: total cells, lymphocytes, neutrophils, macrophages
  • Bal cytokines measures: IFNγ, IL-1β, IL-4, IL-5, IL-6, KC/GRO, TNFα
  • Histology of left lung, and slides stained as follows:
    • H&E stain for semiquantitative histological analysis
    • Trichrome stain for collagen deposition

Citations

Thompson, J.A., Johnston, R.A., R.E. Price, A.F. Hubbs^, J.S., Kashon, McKinney, W., and Fedan, J.S., (2021). High-Fat Western Diet Consumption Exacerbates Silica-Induced Pulmonary Inflammation and Fibrosis. Toxicology Reports 9 (2022) 1045-1053.

Acknowledgements

This work was supported by the Centers for Disease Control and Prevention. The authors wish to acknowledge the facilities, maintenance, and security personnel of NIOSH Morgantown for the hard-work and dedication they provided which was integral in the completion of this work.

When a publication makes use of this data set, acknowledgement of the development of the data set should be attributed to National Institute for Occupational Safety and Health (NIOSH), Health Effects Laboratory Division (HELD).

Funding for this project was provided by the National Institute for Occupational Safety and Health.

Contact

For further information contact:

Pathology and Physiology Research Branch (PPRB), Health Effects Lab Division (HELD),
National Institute for Occupational Safety and Health (NIOSH), Morgantown, WV.
304.285.5831