Quantitative Analysis of Serum Autotaxin Levels in Asthma and Chronic Obstructive Pulmonary Disease.

Duff, RF; Emo, Jason; Friedman, Alan E.; Larj, Michael J.; Lyda, Elizabeth; O'Loughlin, Colm; Rahman, Irfan; Block, Robert C.; Morris, Andrea; Prestwich, Glenn D.; Georas, SN

doi:10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2528

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“…The relative contributions of AGK and/or PLD pathways in LPA generation in response to Schistosoma mansoni eggs sensitization and challenge are unknown Additionally, extracellular LPA can be generated by lysoPLD (autotaxin), which converts lysophosphatidylcholine (LPC) to LPA [ 50 ]. Not only LPC levels were increased in BAL fluids of segmental allergen challenged patients [ 51 ], there was an increase in lysoPLD expression in LPS-stimulated monocytes [ 52 ], and stimulation of lysoPLD activity in asthmatic patients [ 53 ]. Thus, increase in LPC levels and lysoPLD expression and activity may be involved in enhanced LPA generation during lung inflammation.…”

Section: Discussionmentioning

confidence: 99%

Role of lysophosphatidic acid receptor LPA2 in the development of allergic airway inflammation in a murine model of asthma

Zhao

Tong

et al. 2009

Respir Res

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BackgroundLysophosphatidic acid (LPA) plays a critical role in airway inflammation through G protein-coupled LPA receptors (LPA1-3). We have demonstrated that LPA induced cytokine and lipid mediator release in human bronchial epithelial cells. Here we provide evidence for the role of LPA and LPA receptors in Th2-dominant airway inflammation.MethodsWild type, LPA1 heterozygous knockout mice (LPA1+/-), and LPA2 heterozygous knockout mice (LPA2+/-) were sensitized with inactivated Schistosoma mansoni eggs and local antigenic challenge with Schistosoma mansoni soluble egg Ag (SEA) in the lungs. Bronchoalveolar larvage (BAL) fluids and lung tissues were collected for analysis of inflammatory responses. Further, tracheal epithelial cells were isolated and challenged with LPA.ResultsBAL fluids from Schistosoma mansoni egg-sensitized and challenged wild type mice (4 days of challenge) showed increase of LPA level (~2.8 fold), compared to control mice. LPA2+/- mice, but not LPA1+/- mice, exposed to Schistosoma mansoni egg revealed significantly reduced cell numbers and eosinophils in BAL fluids, compared to challenged wild type mice. Both LPA2+/- and LPA1+/- mice showed decreases in bronchial goblet cells. LPA2+/- mice, but not LPA1+/- mice showed the decreases in prostaglandin E2 (PGE2) and LPA levels in BAL fluids after SEA challenge. The PGE2 production by LPA was reduced in isolated tracheal epithelial cells from LPA2+/- mice. These results suggest that LPA and LPA receptors are involved in Schistosoma mansoni egg-mediated inflammation and further studies are proposed to understand the role of LPA and LPA receptors in the inflammatory process.

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