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Dietary ω-6 polyunsaturated fatty acid arachidonic acid increases inflammation, but inhibits ECM protein expression in COPD.
Respir Res. 2018 Nov 03; 19(1):211.RR

Abstract

BACKGROUND

The obesity paradox in COPD describes protective effects of obesity on lung pathology and inflammation. However, the underlying relationships between obesity, diet and disease outcomes in COPD are not fully understood. In this study we measured the response to dietary fatty acids upon markers of inflammation and remodelling in human lung cells from people with and without COPD.

METHODS

Pulmonary fibroblasts were challenged with ω-3 polyunsaturated fatty acids (PUFAs), ω-6 PUFAs, saturated fatty acids (SFAs) or the obesity-associated cytokine TNFα. After 48-72 h release of the pro-inflammatory cytokines interleukin (IL)-6 and CXCL8 was measured using ELISA and mRNA expression and deposition of the extracellular matrix (ECM) proteins fibronectin, type I collagen, tenascin and perlecan were measured using qPCR or ECM ELISA, respectively.

RESULTS

Challenge with the ω-6 PUFA arachidonic acid (AA), but not ω-3 PUFAs or SFAs, resulted in increased IL-6 and CXCL8 release from fibroblasts, however IL-6 and CXCL8 release was reduced in COPD (n = 19) compared to non-COPD (n = 36). AA-induced cytokine release was partially mediated by downstream mediators of cyclooxygenase (COX)-2 in both COPD and non-COPD. In comparison, TNFα-induced IL-6 and CXCL8 release was similar in COPD and non-COPD, indicating a specific interaction of AA in COPD. In patients with or without COPD, regression analysis revealed no relationship between BMI and cytokine release. In addition, AA, but not SFAs or ω-3 PUFAs reduced the basal deposition of fibronectin, type I collagen, tenascin and perlecan into the ECM in COPD fibroblasts. In non-COPD fibroblasts, AA-challenge decreased basal deposition of type I collagen and perlecan, but not fibronectin and tenascin.

CONCLUSIONS

This study shows that AA has disease-specific effects on inflammation and ECM protein deposition. The impaired response to AA in COPD might in part explain why obesity appears to have less detrimental effects in COPD, compared to other lung diseases.

Authors+Show Affiliations

Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia. Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute and The University of Newcastle, Newcastle, NSW, Australia.Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia. School of Life Sciences, University of Technology Sydney, Sydney, Australia.Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia.Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute and The University of Newcastle, Newcastle, NSW, Australia.Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia.Priority Research Centre for Healthy Lungs, Hunter Medical Research Institute and The University of Newcastle, Newcastle, NSW, Australia.Respiratory Cellular and Molecular Biology, Woolcock Institute of Medical Research, The University of Sydney, Sydney, Australia. brian.oliver@uts.edu.au. School of Life Sciences, University of Technology Sydney, Sydney, Australia. brian.oliver@uts.edu.au.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30390648

Citation

Rutting, Sandra, et al. "Dietary Ω-6 Polyunsaturated Fatty Acid Arachidonic Acid Increases Inflammation, but Inhibits ECM Protein Expression in COPD." Respiratory Research, vol. 19, no. 1, 2018, p. 211.
Rutting S, Papanicolaou M, Xenaki D, et al. Dietary ω-6 polyunsaturated fatty acid arachidonic acid increases inflammation, but inhibits ECM protein expression in COPD. Respir Res. 2018;19(1):211.
Rutting, S., Papanicolaou, M., Xenaki, D., Wood, L. G., Mullin, A. M., Hansbro, P. M., & Oliver, B. G. (2018). Dietary ω-6 polyunsaturated fatty acid arachidonic acid increases inflammation, but inhibits ECM protein expression in COPD. Respiratory Research, 19(1), 211. https://doi.org/10.1186/s12931-018-0919-4
Rutting S, et al. Dietary Ω-6 Polyunsaturated Fatty Acid Arachidonic Acid Increases Inflammation, but Inhibits ECM Protein Expression in COPD. Respir Res. 2018 Nov 3;19(1):211. PubMed PMID: 30390648.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary ω-6 polyunsaturated fatty acid arachidonic acid increases inflammation, but inhibits ECM protein expression in COPD. AU - Rutting,Sandra, AU - Papanicolaou,Michael, AU - Xenaki,Dia, AU - Wood,Lisa G, AU - Mullin,Alexander M, AU - Hansbro,Philip M, AU - Oliver,Brian G, Y1 - 2018/11/03/ PY - 2018/07/18/received PY - 2018/10/21/accepted PY - 2018/11/5/entrez PY - 2018/11/6/pubmed PY - 2019/1/24/medline KW - Airway inflammation KW - COPD KW - Human pulmonary fibroblasts KW - Remodelling KW - ω-6 PUFAs SP - 211 EP - 211 JF - Respiratory research JO - Respir. Res. VL - 19 IS - 1 N2 - BACKGROUND: The obesity paradox in COPD describes protective effects of obesity on lung pathology and inflammation. However, the underlying relationships between obesity, diet and disease outcomes in COPD are not fully understood. In this study we measured the response to dietary fatty acids upon markers of inflammation and remodelling in human lung cells from people with and without COPD. METHODS: Pulmonary fibroblasts were challenged with ω-3 polyunsaturated fatty acids (PUFAs), ω-6 PUFAs, saturated fatty acids (SFAs) or the obesity-associated cytokine TNFα. After 48-72 h release of the pro-inflammatory cytokines interleukin (IL)-6 and CXCL8 was measured using ELISA and mRNA expression and deposition of the extracellular matrix (ECM) proteins fibronectin, type I collagen, tenascin and perlecan were measured using qPCR or ECM ELISA, respectively. RESULTS: Challenge with the ω-6 PUFA arachidonic acid (AA), but not ω-3 PUFAs or SFAs, resulted in increased IL-6 and CXCL8 release from fibroblasts, however IL-6 and CXCL8 release was reduced in COPD (n = 19) compared to non-COPD (n = 36). AA-induced cytokine release was partially mediated by downstream mediators of cyclooxygenase (COX)-2 in both COPD and non-COPD. In comparison, TNFα-induced IL-6 and CXCL8 release was similar in COPD and non-COPD, indicating a specific interaction of AA in COPD. In patients with or without COPD, regression analysis revealed no relationship between BMI and cytokine release. In addition, AA, but not SFAs or ω-3 PUFAs reduced the basal deposition of fibronectin, type I collagen, tenascin and perlecan into the ECM in COPD fibroblasts. In non-COPD fibroblasts, AA-challenge decreased basal deposition of type I collagen and perlecan, but not fibronectin and tenascin. CONCLUSIONS: This study shows that AA has disease-specific effects on inflammation and ECM protein deposition. The impaired response to AA in COPD might in part explain why obesity appears to have less detrimental effects in COPD, compared to other lung diseases. SN - 1465-993X UR - https://www.unboundmedicine.com/medline/citation/30390648/Dietary_ω_6_polyunsaturated_fatty_acid_arachidonic_acid_increases_inflammation_but_inhibits_ECM_protein_expression_in_COPD_ L2 - https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-018-0919-4 DB - PRIME DP - Unbound Medicine ER -