Journal of Applied Physiology
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J Appl Physiol (January 11, 2002). doi:10.1152/japplphysiol.00927.2001
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Articles in PresS, published online ahead of print January 11, 2002
J Appl Physiol, 10.1152/jap.00927.2001
Submitted on September 6, 2001
Accepted on January 9, 2002

Characterization of LPS-induced lung inflammation in cftr-/- mice and the effect of docosahexaenoic acid

Steven D Freedman*, Deborah Weinstein, Paola G Blanco, Pedro Martinez-lark, Serge Urman, Munir Zaman, Jason D Morrow, and Juan G Alvarez

* To whom correspondence should be addressed. E-mail: sfreedma{at}caregroup.harvard.edu.

The mechanism by which Pseudomonas causes excessive inflammation in the cystic fibrosis lung is unclear. We've reported that arachidonic acid is increased and docosahexaenoic acid (DHA) decreased in lung, pancreas, and ileum from cftr-/- mice. Oral DHA corrected this defect and reversed the pathology. To determine which mediators regulate inflammation in lungs from cftr-/- mice and whether inhibition occurs with DHA, cftr-/- and wild-type (WT) mice were exposed to aerosolized Pseudomonas LPS. After 2 days of LPS, TNF-{alpha}, MIP-2 and KC levels in bronchoalveolar lavage (BAL) fluid were increased in cftr-/- compared to WT mice and not suppressed by pretreatment with oral DHA. Neutrophil levels were not different between cftr-/- and WT mice. After 3 days of aerosolized LPS, neutrophil concentration, TNF-{alpha}, the eicosanoids 6-keto PGF1{alpha} PGF2{alpha} PGE2 and thromboxane B2 were all increaed in BAL fluid from cftr-/- mice compared to WT controls. Oral DHA has no significant effect on TNF-{alpha} levels in cftr-/- mice. In contrast, neutrophils and eicosanoids were decreased in cftr-/- but not in WT mice treated with DHA indicating that the effects of DHA on these inflammatory parameters may be related to correction of the membrane lipid defect.




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