Skip to main content

Some NLM-NCBI services and products are experiencing heavy traffic, which may affect performance and availability. We apologize for the inconvenience and appreciate your patience. For assistance, please contact our Help Desk at info@ncbi.nlm.nih.gov.

Mediators of Inflammation logoLink to Mediators of Inflammation
. 2001 Feb;10(1):21–26. doi: 10.1080/09629350123056

Effects of fluticasone propionate inhalation on levels of arachidonic acid metabolites in patients with chronic obstructive pulmonary disease.

G T Verhoeven 1, I M Garrelds 1, H C Hoogsteden 1, F J Zijlstra 1
PMCID: PMC1781690  PMID: 11324900

Abstract

BACKGROUND: In smoking COPD patients the bronchoalveolar lavage (BAL) fluid contains high numbers of inflammatory cells. These cells might produce arachidonic acid (AA) metabolites, which contribute to inflammation and an increased bronchomotor tone. AIMS: To investigate levels of AA metabolites in BAL fluid, before and after inhaled glucocorticoid therapy: fluticasone propionate (FP) 1 mg per day, or placebo. METHODS: A double-blind placebo controlled trial lasting six months. COPD patients were selected by clinical criteria and the presence of bronchial hyper-responsiveness (BHR). Lung function was recorded and in BAL fluid we counted cell numbers and measured LTB4, LTC4/D4/E4, PGE2, 6kPGF1alpha, PGF2alpha and TxB2. A control group consisted of asymptomatic smokers (n=6). RESULTS: Paired data were obtained from 9 FP treated and 11 placebo patients. BAL cells were almost exclusively alveolar macrophages. In patients and controls both cellularity and levels of AA metabolites were equal Cell numbers did not change after treatment. Statistically significant decreases after FP therapy were noticed for PGE2 (30%), 6kPGF1alpha (41%) and PGF2alpha (54%). CONCLUSIONS: In COPD, the capability of inflammatory cells to produce certain AA metabolites was decreased after inhaled FP treatment. This result is discussed in its relation to clinical effects, the influence of smoking, and the results of an earlier, similar study in asthma patients.

Full Text

The Full Text of this article is available as a PDF (148.2 KB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Beasley R., Varley J., Robinson C., Holgate S. T. Cholinergic-mediated bronchoconstriction induced by prostaglandin D2, its initial metabolite 9 alpha,11 beta-PGF2, and PGF2 alpha in asthma. Am Rev Respir Dis. 1987 Nov;136(5):1140–1144. doi: 10.1164/ajrccm/136.5.1140. [DOI] [PubMed] [Google Scholar]
  2. Fedi P., Calabrò A., Orsini B., Milani S., Zacchi P., Salvadori G., Surrenti C. Cigarette smoking increases gastric luminal prostaglandin F2 alpha and thromboxane B2 in healthy smokers. Digestion. 1990;46(1):27–34. doi: 10.1159/000200275. [DOI] [PubMed] [Google Scholar]
  3. Jeffery P. K. Comparison of the structural and inflammatory features of COPD and asthma. Giles F. Filley Lecture. Chest. 2000 May;117(5 Suppl 1):251S–260S. doi: 10.1378/chest.117.5_suppl_1.251s. [DOI] [PubMed] [Google Scholar]
  4. Lee L. Y., Hong J. L. Involvement of prostanoids in cigarette smoking-induced pathophysiological effects in the lung. Prostaglandins Leukot Essent Fatty Acids. 1999 Sep;61(3):145–155. doi: 10.1054/plef.1999.0084. [DOI] [PubMed] [Google Scholar]
  5. Quanjer P. H., Tammeling G. J., Cotes J. E., Pedersen O. F., Peslin R., Yernault J. C. Lung volumes and forced ventilatory flows. Report Working Party Standardization of Lung Function Tests, European Community for Steel and Coal. Official Statement of the European Respiratory Society. Eur Respir J Suppl. 1993 Mar;16:5–40. [PubMed] [Google Scholar]
  6. Richter M., Sirois P. Effects of eicosanoids, neuromediators and bioactive peptides on murine airways. Eur J Pharmacol. 2000 Feb 18;389(2-3):225–234. doi: 10.1016/s0014-2999(99)00878-x. [DOI] [PubMed] [Google Scholar]
  7. Rijcken B., Schouten J. P., Xu X., Rosner B., Weiss S. T. Airway hyperresponsiveness to histamine associated with accelerated decline in FEV1. Am J Respir Crit Care Med. 1995 May;151(5):1377–1382. doi: 10.1164/ajrccm.151.5.7735588. [DOI] [PubMed] [Google Scholar]
  8. Saetta M. Airway inflammation in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1999 Nov;160(5 Pt 2):S17–S20. doi: 10.1164/ajrccm.160.supplement_1.6. [DOI] [PubMed] [Google Scholar]
  9. Tashkin D. P., Altose M. D., Connett J. E., Kanner R. E., Lee W. W., Wise R. A. Methacholine reactivity predicts changes in lung function over time in smokers with early chronic obstructive pulmonary disease. The Lung Health Study Research Group. Am J Respir Crit Care Med. 1996 Jun;153(6 Pt 1):1802–1811. doi: 10.1164/ajrccm.153.6.8665038. [DOI] [PubMed] [Google Scholar]
  10. Zijlstra F. J., Vincent J. E., Mol W. M., Hoogsteden H. C., Van Hal P. T., Jongejan R. C. Eicosanoid levels in bronchoalveolar lavage fluid of young female smokers and non-smokers. Eur J Clin Invest. 1992 May;22(5):301–306. doi: 10.1111/j.1365-2362.1992.tb01466.x. [DOI] [PubMed] [Google Scholar]

Articles from Mediators of Inflammation are provided here courtesy of Wiley

RESOURCES