Inducible cyclooxygenase released prostaglandin E2 modulates the severity of infection caused by Streptococcus pyogenes

The Journal of Immunology : Official Journal of the American Association of Immunologists
Oliver GoldmannEva Medina

Abstract

Streptococcus pyogenes is a significant human pathogen that can cause life-threatening invasive infections. Understanding the mechanism of disease is crucial to the development of more effective therapies. In this report, we explored the role of PGE(2), an arachidonic acid metabolite, and its rate-limiting enzyme cyclooxygenase 2 (COX-2) in the pathogenesis of severe S. pyogenes infections. We found that the COX-2 expression levels in tissue biopsies from S. pyogenes-infected patients, as well as in tissue of experimentally infected mice, strongly correlated with the severity of infection. This harmful effect was attributed to PGE(2)-mediated suppression of the bactericidial activity of macrophages through interaction with the G2-coupled E prostanoid receptor. The suppressive effect of PGE(2) was associated with enhanced intracellular cAMP production and was mimicked by the cAMP-elevating agent, forskolin. Activation of protein kinase A (PKA) was the downstream effector mechanisms of cAMP because treatment with PKI(14-22), a highly specific inhibitor of PKA, prevented the PGE(2)-mediated inhibition of S. pyogenes killing in macrophages. The inhibitory effect exerted by PKA in the generation of antimicrobial oxygen radical speci...Continue Reading

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