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5‐Lipoxygenase knockout mice exhibit a resistance to pleurisy and lung injury caused by carrageenan
Author(s) -
Cuzzocrea Salvatore,
Rossi Antonietta,
Serraino Ivana,
Mazzon Emanuela,
Di Paola Rosanna,
Dugo Laura,
Genovese Tiziana,
Calabrò Barbara,
Caputi Achille P.,
Sautebin Lidia
Publication year - 2003
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.1002477
Subject(s) - pleurisy , carrageenan , inflammation , infiltration (hvac) , myeloperoxidase , biology , lung , intercellular adhesion molecule 1 , knockout mouse , pathology , selectin , immunology , medicine , biochemistry , pleural effusion , receptor , physics , thermodynamics
In the present study, by comparing the responses in wild‐type (WT) mice and mice lacking [knockout (KO)] the 5‐lipoxygenase (5‐LO), we investigated the role played by 5‐LO in the development of acute inflammation. When compared with carragenan‐treated 5‐LOWT mice, 5‐LOKO mice, which had received carrageenan, exhibited a reduced degree of pleural exudation, polymorphonuclear cell migration. Lung myeloperoxidase activity, an index of neutrophil infiltration, was significantly reduced in 5‐LOKO mice in comparison with 5‐LOWT. Lung‐tissue sections from carrageenan‐treated 5‐LOWT mice showed positive staining for intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), P‐selectin, and E‐selectin, which were mainly localized around vessels. The intensity and degree of ICAM‐1, VCAM‐1, P‐selectin, and E‐selectin were markedly reduced in tissue section from carrageenan‐5‐LOKO mice, which also improved the histological status of the inflamed lungs. Taken together, our results clearly demonstrate that 5‐LO modulates neutrophil infiltration in the acute lung inflammation.

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