Oleic Acid Induces Lung Injury in Mice through Activation of the ERK Pathway

• Main Authors: Cassiano Felippe Gonçalves-de-Albuquerque, Adriana Ribeiro Silva, Patrícia Burth, Isabel Matos Medeiros de Moraes, Flora Magno de Jesus Oliveira, Mauricio Younes-Ibrahim, Maria da Conceição Batista dos Santos, Heloísa D’Ávila, Patrícia Torres Bozza, Hugo Caire de Castro Faria Neto, Mauro Velho de Castro Faria
• Format: Article
• Language: English
• Published: Hindawi Limited 2012-01-01
• Series: Mediators of Inflammation
• Online Access: http://dx.doi.org/10.1155/2012/956509

Oleic acid (OA) can induce acute lung injury in experimental models. In the present work, we used intratracheal OA injection to show augmented oedema formation, cell migration and activation, lipid mediator, and cytokine productions in the bronchoalveolar fluids of Swiss Webster mice. We also demonstrated that OA-induced pulmonary injury is dependent on ERK1/2 activation, since U0126, an inhibitor of ERK1/2 phosphorylation, blocked neutrophil migration, oedema, and lipid body formation as well as IL-6, but not IL-1β production. Using a mice strain carrying a null mutation for the TLR4 receptor, we proved that increased inflammatory parameters after OA challenges were not due to the activation of the TLR4 receptor. With OA being a Na/K-ATPase inhibitor, we suggest the possible involvement of this enzyme as an OA target triggering lung inflammation.