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Temporal lipid mediator profiles differ between plasma and bronchoalveolar lavage in mice exposed to tobacco smoke
Author(s) -
Nording Malin Linder,
Yang Jun,
Hoang Laura,
Zamora Vanessa,
Uyeminami Dale,
Espiritu Imelda,
Pinkerton Kent E.,
Hammock Bruce D.,
Luria Ayala
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.668.3
Subject(s) - oxylipin , bronchoalveolar lavage , chemistry , inflammation , tobacco smoke , cytochrome p450 , lipoxygenase , respiratory tract , lipid signaling , pharmacology , immunology , respiratory system , metabolism , biochemistry , medicine , lung , enzyme , polymer chemistry
Patients with chronic obstructive pulmonary disease exhibit inflammation in the respiratory tract. In order to investigate temporal trends of the inflammatory response, a murine model of short‐term tobacco smoke (TS) exposure was used. Focus was on lipid mediators in the oxylipin family, i.e. oxidized fatty acids including eicosanoids of the cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP) metabolic pathways. Mice (C57Bl/6) were exposed to TS for 3, 9, and 15 hours, or filtered air (FA). Bronchoalveolar lavage fluid (BALF) and plasma samples underwent solid phase extraction followed by analysis with liquid chromatography coupled to tandem mass spectrometry. The resulting oxylipin levels were higher in plasma than in BALF, and a larger number of oxylipins was detected in plasma than in BALF (28 vs 21). Furthermore, the fraction of LOX‐derived oxylipins was the same, while the fraction of COX‐ and CYP‐derived oxylipins differed between BALF and plasma. Six of the LOX‐oxylipins in BALF, and none in plasma, were significantly increased after 9h of TS exposure correlating to a significant increase in total number of infiltrated cells ( p=0.05 ). In conclusion, temporal oxylipin profiles may be used to assess the progression of pulmonary inflammation in mice exposed to TS. TRDRP 16KT‐0037, NIEHS Grants ES02710, P42 ES04699, and the Swedish Research Councils VR, Formas, and Vinnova supported this work.