Therapeutic treatment of dietary docosahexaenoic acid for particle-induced pulmonary inflammation in Balb/c mice

Paige Fletcher, Raymond F. Hamilton, Joseph F. Rhoderick, Britten Postma, Mary Buford, James J. Pestka, Andrij Holian

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Objective and design: The omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA) has been reported to suppress inflammation. Pulmonary inflammation can be directly linked to exposure of various occupational and man-made particles leading to pulmonary diseases. Therapeutic treatments are lacking for particle-induced pulmonary inflammation. These studies evaluated DHA as a therapeutic treatment for semi-acute and chronic particle-induced pulmonary inflammation. Methods: Balb/c mice were oropharyngeal instilled with hydrophobic multi-walled carbon nanotube (MWCNT) or hydrophilic crystalline silica (SiO2) either as one instillation (semi-acute) or once a week for 4 weeks (chronic). One week later, the mice were placed on either a control or 1% DHA-containing diet for 3 weeks (semi-acute) or 12 weeks (chronic). Mice were assessed for inflammatory signaling within the lung lavage fluid, impact on phagolysosomal membrane permeability, shifts of macrophage phenotype gene expression (M1, M2a, M2b, and M2c), and pulmonary histopathology. Results: DHA increased pulmonary inflammatory markers and lung pathology when mice were exposed to SiO2. There were trending decreases of inflammatory markers for MWCNT-exposed mice with DHA treatment, however, mostly not statistically significant. Conclusion: The anti-inflammatory benefits of DHA treatment depend upon the type of inflammatory particle, magnitude of inflammation, and duration of treatment.

Original languageEnglish
Pages (from-to)359-373
Number of pages15
JournalInflammation Research
Volume70
Issue number3
DOIs
StatePublished - Mar 2021

Keywords

  • Crystalline silica
  • Docosahexaenoic acid
  • Macrophage phenotype
  • Multi-walled carbon nanotube
  • Phagolysosomal membrane damage
  • Pulmonary inflammation

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