Literature DB >> 34655011

Dietary Docosahexaenoic Acid as a Potential Treatment for Semi-acute and Chronic Particle-Induced Pulmonary Inflammation in Balb/c Mice.

Paige Fletcher1, Raymond F Hamilton2, Joseph F Rhoderick2, Britten Postma2, Mary Buford2, James J Pestka3, Andrij Holian2.   

Abstract

Acute and chronic inflammation are vital contributing factors to pulmonary diseases which can be triggered by exposure to occupational and man-made particles; however, there are no established treatments. One potential treatment shown to have anti-inflammatory capabilities is the dietary supplement docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid found in fish oil. DHA's anti-inflammatory mechanisms are unclear for particle-induced inflammation; therefore, this study evaluated DHA as a prophylactic treatment for semi-acute and chronic particle-induced inflammation in vivo. Balb/c mice were fed a control or 1% DHA diet and exposed to dispersion media, an inflammatory multi-walled carbon nanotube (MWCNT), or crystalline silica (SiO2) either once (semi-acute) or once a week for 4 weeks (chronic). The hypothesis was that DHA will decrease pulmonary inflammatory markers in response to particle-induced inflammation. Results indicated that DHA had a trending anti-inflammatory effect in mice exposed to MWCNT. There was a general decrease in inflammatory signals within the lung lavage fluid and upregulation of M2c macrophage gene expression in the spleen tissue. In contrast, mice exposed to SiO2 while on the DHA diet significantly increased most inflammatory markers. However, DHA stabilized the phagolysosomal membrane upon prolonged treatment. This indicated that DHA treatment may depend upon certain inflammatory particle exposures as well as the length of the exposure.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  alveolar macrophage; crystalline silica; macrophage phenotype; multi-walled carbon nanotube; phagolysosomal membrane damage; pulmonary inflammation

Mesh:

Substances:

Year:  2021        PMID: 34655011      PMCID: PMC8957518          DOI: 10.1007/s10753-021-01576-y

Source DB:  PubMed          Journal:  Inflammation        ISSN: 0360-3997            Impact factor:   4.092


  56 in total

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