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Published on: December 17, 2011
PGE(2) suppression of innate immunity during mucosal bacterial infection
Mallory Agard1, Saja Asakrah, Lisa A Morici
1Department of Microbiology and Immunology, Tulane University School of Medicine New Orleans, LA 70119, USA.
Abstract:
Prostaglandin E2 (PGE2) is an important lipid mediator in inflammatory and immune responses during acute and chronic infections. Upon stimulation by various proinflammatory stimuli such as lipopolysaccharide (LPS), interleukin (IL)-1β, and tumor necrosis factor (TNF)-α, PGE2 synthesis is upregulated by the expression of cyclooxygenases. Biologically active PGE2 is then able to signal through four primary receptors to elicit a response. PGE2 is a critical molecule that regulates the activation, maturation, migration, and cytokine secretion of several immune cells, particularly those involved in innate immunity such as macrophages, neutrophils, natural killer cells, and dendritic cells. Both Gram-negative and Gram-positive bacteria can induce PGE2 synthesis to regulate immune responses during bacterial pathogenesis. This review will focus on PGE2 in innate immunity and how bacterial pathogens influence PGE2 production during enteric and pulmonary infections. The conserved ability of many bacterial pathogens to promote PGE2 responses during infection suggests a common signaling mechanism to deter protective pro-inflammatory immune responses. Inhibition of PGE2 production and signaling during infection may represent a therapeutic alternative to treat bacterial infections. Further study of the immunosuppressive effects of PGE2 on innate immunity will lead to a better understanding of potential therapeutic targets within the PGE2 pathway.
Insights
Prostaglandin E2 (PGE2) is a key mediator in immune responses to bacterial infections. This molecule can suppress innate immunity, suggesting therapeutic potential for inhibiting its production.
Area of Science:
- Immunology
- Microbiology
- Biochemistry
Background:
- Prostaglandin E2 (PGE2) is a lipid mediator crucial for inflammatory and immune responses.
- PGE2 synthesis is upregulated by pro-inflammatory stimuli like LPS, IL-1β, and TNF-α via cyclooxygenase expression.
- PGE2 signals through four receptors, regulating immune cell functions and cytokine secretion.
Purpose of the Study:
- To review the role of PGE2 in innate immunity during bacterial infections.
- To explore how bacterial pathogens influence PGE2 production in enteric and pulmonary infections.
- To discuss the potential of targeting the PGE2 pathway for therapeutic interventions.
Main Methods:
- Literature review focusing on Prostaglandin E2 (PGE2) in innate immunity.
- Analysis of bacterial pathogen influence on PGE2 production during infections.
- Examination of immunosuppressive effects of PGE2 on immune cells.
Main Results:
- PGE2 regulates the activation, maturation, migration, and cytokine secretion of innate immune cells (macrophages, neutrophils, NK cells, dendritic cells).
- Both Gram-negative and Gram-positive bacteria induce PGE2 synthesis to modulate immune responses during pathogenesis.
- Bacterial pathogens commonly promote PGE2 responses, potentially to evade protective pro-inflammatory immunity.
Conclusions:
- PGE2 plays a significant role in innate immunity during bacterial infections.
- Targeting PGE2 production or signaling may offer a therapeutic strategy against bacterial infections.
- Further research into PGE2's immunosuppressive effects can identify novel therapeutic targets.
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