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Updated: Jun 8, 2026
Isolation of Murine Peritoneal Macrophages to Carry Out Gene Expression Analysis Upon Toll-like Receptors Stimulation
Published on: April 29, 2015
Role of prostaglandin E2 in peptidoglycan mediated iNOS expression in mouse peritoneal macrophages in vitro
Yogesh Dahiya1, Rajeev Kumar Pandey, Kunal H Bhatt
1School of Biotechnology, Faculty of Science, Banaras Hindu University, Varanasi, India.
Abstract:
Many extracellular stimuli, e.g. microbial products, cytokines etc., result in the expression of inducible nitric oxide synthase (iNOS) in macrophages. However, it is not known whether expression of the iNOS gene in response to microbial products is a primary response of macrophages, or is the result of paracrine/autocrine signalling induced by endogenous biomolecules that are synthesised as a result of host cell-microbe interaction. In this paper we demonstrate that iNOS expression in mouse peritoneal macrophages in response to bacterial peptidoglycan (PGN) is a secondary effect requiring autocrine signalling of endogenously produced prostaglandin E2, and that PGN stimulation is mandatory, but not sufficient in itself, for induction of iNOS expression.
Insights
Bacterial peptidoglycan (PGN) triggers inducible nitric oxide synthase (iNOS) expression in macrophages, but this requires autocrine signaling via prostaglandin E2. PGN stimulation is essential but not sufficient for iNOS gene induction.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Extracellular stimuli like microbial products and cytokines induce inducible nitric oxide synthase (iNOS) in macrophages.
- The mechanism of iNOS gene expression in response to microbial products remains unclear, specifically whether it's a primary response or mediated by signaling pathways.
Purpose of the Study:
- To investigate whether inducible nitric oxide synthase (iNOS) gene expression in macrophages stimulated by bacterial peptidoglycan (PGN) is a primary response or a secondary effect mediated by autocrine/paracrine signaling.
Main Methods:
- Primary mouse peritoneal macrophages were stimulated with bacterial peptidoglycan (PGN).
- The role of endogenously produced prostaglandin E2 (PGE2) in mediating iNOS expression was assessed.
Main Results:
- Inducible nitric oxide synthase (iNOS) expression in mouse peritoneal macrophages following bacterial peptidoglycan (PGN) stimulation is a secondary effect.
- This induction is dependent on autocrine signaling involving endogenously produced prostaglandin E2 (PGE2).
- PGN stimulation is a necessary but insufficient condition for iNOS expression.
Conclusions:
- Inducible nitric oxide synthase (iNOS) expression in macrophages upon encountering bacterial peptidoglycan (PGN) is not a direct primary response.
- Autocrine signaling through prostaglandin E2 (PGE2) is crucial for mediating iNOS induction following PGN stimulation.
- Combined PGN stimulation and autocrine PGE2 signaling are required for iNOS gene expression in macrophages.
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