Cited by 109Inflammatory mediators and NSAID effectsImmune Response and InflammationEicosanoids and Hypertension Pharmacology

Prostaglandin E 2 as a Regulator of Immunity to Pathogens

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Martínez-Colón, Giovanny J., Moore, Bethany B.·2018·Pharmacology & Therapeutics

Abstract

The body is exposed to foreign pathogens every day, but remarkably, most pathogens are effectively cleared by the innate immune system without the need to invoke the adaptive immune response. Key cellular components of the innate immune system include macrophages and neutrophils and the recruitment and function of these cells are tightly regulated by chemokines and cytokines in the tissue space. Innate immune responses are also known to regulate development of adaptive immune responses often via the secretion of various cytokines. In addition to these protein regulators, numerous lipid mediators can also influence innate and adaptive immune functions. In this review, we cover one particular lipid regulator, prostaglandin E 2 (PGE 2) and describe its synthesis and signaling and what is known about the ability of this lipid to regulate immunity and host defense against viral, fungal and bacterial pathogens.

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Crossref · 10.1016/j.pharmthera.2017.12.008

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  • PGE2 is an arachadonic acid metabolite with roles in ILC2, T helper cell, macrophage, dendritic cell, and neutrophil responses.

    “PGE2 is an arachadonic acid metabolite, with roles in ILC2, T helper cell, macrophage, dendritic cell, and neutrophil responses (Martínez-Colón and Moore, 2018).”

    From Modulation of Host Immunity by Helminths: The Expanding Repertoire of Parasite Effector Molecules (2018) · cites this paper as Martínez-Colón and Moore, 2018

    The PGE2 synthesis section describes PGE2 as a product of arachidonic acid metabolism. The adaptive-immunity section describes effects on dendritic cells and T-helper responses, while the innate-immune sections describe effects on macrophages and neutrophils. No passage found addresses ILC2 responses (searched: ILC2 and type 2 innate lymphoid cells). Page numbers were unavailable in our copy. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Martínez-Colón, G. J., & Moore, B. B.
Affiliations
University of Michigan (US)
Corresponding author
Moore, Bethany B.
Venue
Pharmacology & Therapeutics
Publisher
Elsevier BV
Published
2018-05
Volume
185
Pages
135-146
ISSN
0163-7258 (ISSN-L)
OpenAlex
W2779758548
Cited by
109
References
6
Citations by year
2026: 9 · 2025: 14 · 2024: 15 · 2023: 8 · 2022: 17 · 2021: 21 · 2020: 16 · 2019: 5 · 2018: 4
FWCI
0.87
Type
journal article
Language
en
Open access
Locations
  • Pharmacology & Therapeutics (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (5t32ai007413-32)
  • National Heart, Lung, and Blood Institute (R01HL119682, R01HL127805)
  • National Institute of General Medical Sciences (R25GM086262)
  • National Institute of Allergy and Infectious Diseases (T32-AI-007413, R01AI117229)
Topics
  • Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
prostaglandin E2, innate immunity, host defense, macrophages, neutrophils, chemokines, cytokines, lipid mediators, viral pathogens, fungal pathogens, pathogenic bacteria, adaptive immune regulation
MeSH terms
Animals, Autophagy, Humans, Immunity, Innate, Infections, Dinoprostone, Toll-Like Receptors, Interleukin-1beta, Adaptive Immunity, Extracellular Traps

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