Skip to main content

03.11.2023 | Original Article

Effect of nitro-conjugated linoleic acid on the inflammatory response of murine macrophages activated with lipopolysaccharide derived from Prevotella intermedia

verfasst von: Jung Eun Lee, Ah Rim Lee, Eun-Young Choi, In Soon Choi, Sung-Jo Kim

Erschienen in: Inflammopharmacology

Einloggen, um Zugang zu erhalten

Abstract

Nitro-conjugated linoleic acid (NO2-CLA) has been observed to manifest salutary signaling responses, including anti-inflammatory and antioxidant properties. Here, the authors have explored the influence and underlying mechanisms of NO2-CLA on the proinflammatory reaction of murine macrophages that were challenged with lipopolysaccharide (LPS) derived from Prevotella intermedia, a putative periodontopathic bacterium. Treatment of LPS-activated RAW264.7 cells with NO2-CLA notably dampened the secretion of iNOS-derived NO, IL-1β and IL-6 as well as their gene expressions and significantly enhanced the markers for M2 macrophage polarization. NO2-CLA promoted the HO-1 expression in cells challenged with LPS, and tin protoporphyrin IX, an HO-1 inhibitor, significantly reversed the NO2-CLA-mediated attenuation of NO secretion, but not IL-1β or IL-6. We found that cells treated with NO2-CLA significantly increased mRNA expression of PPAR-γ compared to control cells, and NO2-CLA significantly reverted the decrease in PPAR-γ mRNA caused by LPS. Nonetheless, antagonists to PPAR-γ were unable to reverse the NO2-CLA-mediated suppression of inflammatory mediators. In addition, NO2-CLA did not alter the p38 and JNK activation elicited by LPS. Both NF-κB reporter activity and IκB-α degradation caused by LPS were notably diminished by NO2-CLA. NO2-CLA was observed to interrupt the nuclear translocation and DNA binding of p50 subunits caused by LPS with no obvious alterations in p65 subunits. Further, NO2-CLA attenuated the phosphorylation of STAT1/3 elicited in response to LPS. We propose that NO2-CLA could be considered as a possible strategy for the therapy of periodontal disease, although additional researches are certainly required to confirm this.
Literatur
Zurück zum Zitat Baker PR, Lin Y, Schopfer FJ, Woodcock SR, Groeger AL, Batthyany C et al (2005) Fatty acid transduction of nitric oxide signaling: multiple nitrated unsaturated fatty acid derivatives exist in human blood and urine and serve as endogenous peroxisome proliferator-activated receptor ligands. J Biol Chem 280:42464–42475. https://​doi.​org/​10.​1074/​jbc.​M504212200 CrossRefPubMed Baker PR, Lin Y, Schopfer FJ, Woodcock SR, Groeger AL, Batthyany C et al (2005) Fatty acid transduction of nitric oxide signaling: multiple nitrated unsaturated fatty acid derivatives exist in human blood and urine and serve as endogenous peroxisome proliferator-activated receptor ligands. J Biol Chem 280:42464–42475. https://​doi.​org/​10.​1074/​jbc.​M504212200 CrossRefPubMed
Zurück zum Zitat Gao JJ, Filla MB, Fultz MJ, Vogel SN, Russell SW, Murphy WJ et al (1998) Autocrine/paracrine IFN-αβ mediates the lipopolysaccharide-induced activation of transcription factor Stat1α in mouse macrophages: pivotal role of Stat1α in induction of the inducible nitric oxide synthase gene. J Immunol 161:4803–4810 CrossRefPubMed Gao JJ, Filla MB, Fultz MJ, Vogel SN, Russell SW, Murphy WJ et al (1998) Autocrine/paracrine IFN-αβ mediates the lipopolysaccharide-induced activation of transcription factor Stat1α in mouse macrophages: pivotal role of Stat1α in induction of the inducible nitric oxide synthase gene. J Immunol 161:4803–4810 CrossRefPubMed
Zurück zum Zitat Tatakis DN (1993) Interleukin-1 and bone metabolism: a review. J Periodontol 64(5 Suppl):416–431 PubMed Tatakis DN (1993) Interleukin-1 and bone metabolism: a review. J Periodontol 64(5 Suppl):416–431 PubMed
Metadaten
Titel
Effect of nitro-conjugated linoleic acid on the inflammatory response of murine macrophages activated with lipopolysaccharide derived from Prevotella intermedia
verfasst von
Jung Eun Lee
Ah Rim Lee
Eun-Young Choi
In Soon Choi
Sung-Jo Kim
Publikationsdatum
03.11.2023
Verlag
Springer International Publishing
Erschienen in
Inflammopharmacology
Print ISSN: 0925-4692
Elektronische ISSN: 1568-5608
DOI
https://doi.org/10.1007/s10787-023-01340-8