Arachidonic Acid and Docosahexaenoic Acid Metabolites in the Airways of Adults With Cystic Fibrosis: Effect of Docosahexaenoic Acid Supplementation
Teopompi E, Risé P, Pisi R, Buccellati C, Aiello M, Pisi G, Tripodi C, Fainardi V, Clini E, Chetta A, Rovati GE, Sala A
Frontiers in pharmacology · 21 citas
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- Financiación independiente
- Organización sin fines de lucro
- Fondazione per la Ricerca sulla Fibrosi Cistica
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Publicación
- Publicado
- 2019-08-23 · Front Pharmacol · vol. 10 · pág. 938
- Editorial
- Frontiers Media
- Citado
- 24 citas · más que el 80% de estudios similares · 1.5× el promedio de su campo
- Referencias
- 50 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Fatty Acid Research and Health · Respiratory Support and Mechanisms · Cystic Fibrosis Research Advances
- Palabras clave
- Docosahexaenoic acid, Arachidonic acid, Internal medicine, Endocrinology, Leukotriene B4, Leukotriene, Polyunsaturated fatty acid, Fatty acid, Medicine, Chemistry, Biochemistry, Inflammation, Asthma
12 autores
- Elisabetta Teopompi🇮🇹University of Parma
- Patrizia Risé🇮🇹University of Milan
- Roberta Pisi🇮🇹University of Parma
- Carola Buccellati🇮🇹University of Milan
- Marina Aiello🇮🇹University of Parma
- Giovanna Pisi🇮🇹University of Parma
- Candida Tripodi🇮🇹University of Parma
- Valentina Fainardi🇮🇹University of Parma
- Enrico Maria Clini🇮🇹University of Modena and Reggio Emilia
- Alfredo Antonio Chetta🇮🇹University of Parma
- G. Enrico Rovati🇮🇹 · autor de correspondenciaUniversity of Milan
- Angelo Sala🇮🇹University of Milan; Istituto di Biomedicina e di Immunologia Molecolare Alberto Monroy
Resumen
El texto original del estudio, en el idioma en que se publicó.
Cystic fibrosis (CF) is an autosomal recessive disorder, caused by genetic mutations in CF transmembrane conductance regulator protein. Several reports have indicated the presence of specific fatty acid alterations in CF patients, most notably decreased levels of plasmatic and tissue docosahexaenoic acid (DHA), the precursor of specialized pro-resolving mediators. We hypothesized that DHA supplementation could restore the production of DHA-derived products and possibly contribute to a better control of the chronic pulmonary inflammation observed in CF subjects. Sputum samples from 15 CF and 10 chronic obstructive pulmonary disease (COPD) subjects were collected and analyzed by LC/MS/MS, and blood fatty acid were profiled by gas chromatography upon lipid extraction and transmethylation. Interestingly, CF subjects showed increased concentrations of leukotriene B4 (LTB4), prostaglandin E2 (PGE2), and 15-hydroxyeicosatetraenoic acid (15-HETE), when compared with COPD patients, whereas the concentrations of DHA metabolites did not differ between the two groups. After DHA supplementation, not only DHA/arachidonic acid (AA) ratio and highly unsaturated fatty acid index were significantly increased in the subjects completing the study (p 4 and 15-HETE was observed, together with a tendency for a decrease in PGE2, and an increase in 17-hydroxy-docosahexaenoic acid (17OH-DHA) levels. At the end of the washout period, LTB4, PGE2, 15-HETE, and 17OH-DHA showed a trend to return to baseline values. In addition, 15-HETE/17OH-DHA ratio in the same sample significantly decreased after DHA supplementation (p < 0.01) when compared with baseline. In conclusion, our results show here that in CF patients, an impairment in fatty acid metabolism, characterized by increased AA-derived metabolites and decreased DHA-derived metabolites, could be partially corrected by DHA supplementation.
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