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Updated: May 29, 2026
Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages
Published on: February 22, 2017
Prmt2 regulates the lipopolysaccharide-induced responses in lungs and macrophages
Emilie Dalloneau1, Patricia Lopes Pereira, Véronique Brault
1Centre National de la Recherche Scientifique, Institut de Génétique Biologie Moléculaire et Cellulaire, INSERM, Université de Strasbourg, Unité Mixte de Recherche 7104, 67404 Illkirch, France.
Abstract:
Precise control of the LPS stimulation in the lung modulates inflammation and airway hyperresponsiveness involving the well-known TLR4/NF-κB pathway. As a consequence, the expression and secretion of proinflammatory cytokines is tightly regulated with the recruitment of neutrophils. Changes in the LPS-induced responses have been observed in the Prmt2-Col6a1 monosomic model, suggesting the presence of dosage-sensitive genes controlling LPS pathway in the mouse. In this article, we report that the Prmt2 regulates the LPS-induced lung responses in lungs and macrophages. We demonstrate that Prmt2 gene dosage influences the lung airway hyperresponsiveness, the recruitment of neutrophils, and the expression of proinflammatory cytokines, such as IL-6 and TNF-α. In addition, Prmt2 loss of function also altered the nuclear accumulation of NF-κB in stimulated macrophages. Prmt2 should be considered as a new member of the NF-κB pathway controlling LPS-induced inflammatory and lung responses in a dosage-dependent manner, certainly through regulating nuclear accumulation of NF-κB as shown already in fibroblasts.
Insights
This study reveals that Prmt2 gene dosage influences lung inflammation and airway hyperresponsiveness. Prmt2 acts as a new regulator of the lipopolysaccharide (LPS)-induced inflammatory pathway.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Lipopolysaccharide (LPS) stimulation in the lungs triggers inflammation and airway hyperresponsiveness via the Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) pathway.
- Proinflammatory cytokine expression and neutrophil recruitment are key components of LPS-induced lung responses.
- Previous observations in a Prmt2-Col6a1 monosomic model suggested dosage-sensitive genes impacting LPS pathways.
Purpose of the Study:
- To investigate the role of Prmt2 in regulating LPS-induced lung inflammation and airway hyperresponsiveness.
- To determine if Prmt2 gene dosage affects key inflammatory responses.
- To elucidate Prmt2's mechanism of action within the NF-κB signaling pathway.
Main Methods:
- Analysis of LPS-induced lung responses in wild-type and Prmt2-altered mouse models.
- Assessment of airway hyperresponsiveness, neutrophil recruitment, and proinflammatory cytokine (IL-6, TNF-α) expression.
- Evaluation of NF-κB nuclear accumulation in stimulated macrophages.
Main Results:
- Prmt2 gene dosage significantly influences lung airway hyperresponsiveness and neutrophil recruitment following LPS stimulation.
- Prmt2 levels directly impact the expression of proinflammatory cytokines, including IL-6 and TNF-α.
- Loss of Prmt2 function alters the nuclear translocation of NF-κB in LPS-stimulated macrophages.
Conclusions:
- Prmt2 is identified as a novel regulator of LPS-induced lung inflammatory and airway responses.
- Prmt2 exerts its effects in a dosage-dependent manner.
- Prmt2 likely modulates these responses by influencing NF-κB nuclear accumulation, thus acting as a new component of the NF-κB pathway.
