Beverly H Koller

UNCCH, School of Medicine, Genetics

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Prostaglandin E ₂ produced by the lung augments the effector phase of allergic inflammation

Rachel J. Church; Leigh A. Jania; Beverly H. Koller (Profiled Author: Beverly H Koller)

Journal of Immunology. 2012;188(8):4093-4102.

Elevated PGE 2 is a hallmark of most inflammatory lesions. This lipid mediator can induce the cardinal signs of inflammation, and the beneficial actions of nonsteroidal anti-inflammatory drugs are attributed to inhibition of cyclooxygenase (COX)-1 and COX-2, enzymes essential in the biosynthesis of PGE 2 from arachidonic acid. However, both clinical studies and rodent models suggest that, in the asthmatic lung, PGE 2 acts to restrain the immune response and limit physiological change secondary to inflammation. To directly address the role of PGE 2 in the lung, we examined the development of disease in mice lacking microsomal PGE 2 synthase-1 (mPGES1), which converts COX-1/COX-2-derived PGH 2 to PGE 2. We show that mPGES1 determines PGE 2 levels in the naive lung and is required for increases in PGE 2 after OVA-induced allergy. Although loss of either COX-1 or COX-2 increases the disease severity, surprisingly, mPGES1 ^-/- mice show reduced inflammation. However, an increase in serum IgE is still observed in the mPGES1 ^-/- mice, suggesting that loss of PGE 2 does not impair induction of a Th2 response. Furthermore, mPGES1 ^-/- mice expressing a transgenic OVA-specific TCR are also protected, indicating that PGE 2 acts primarily after challenge with inhaled Ag. PGE 2 produced by the lung plays the critical role in this response, as loss of lung mPGES1 is sufficient to protect against disease. Together, this supports a model in which mPGES1-dependent PGE 2 produced by populations of cells native to the lung contributes to the effector phase of some allergic responses. © 2012 by The American Association of Immunologists, Inc.

PMID: 22412193     PMCID: PMC3324636

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