Stearoyl lysophosphatidylcholine enhances the phagocytic ability of macrophages through the AMP-activated protein kinase/p38 mitogen activated protein kinase pathway

Quan, Hui; Hur, Young Hoe; Xin, Chun; Kim, Joungmin; Choi, Jeong-Il; Kim, Man-Young; Bae, Hong-Beom

doi:10.1016/j.intimp.2016.07.014

Cited by 15 publications

(10 citation statements)

References 46 publications

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“…coli in a dose-dependent manner, with a peak effect at a concentration of 3 μM. Because previous studies have shown that p38 MAPK may be involved in macrophage phagocytosis of bacteria [7], [14], we examined whether Rb1 can increase the activity of p38 MAPK in macrophages. Rb1 dose-dependently increased the phosphorylation of p38 MAPK in peritoneal macrophages, and maximal phosphorylation of p38 MAPK was attained at a concentration of 3 μM (Figs.…”

Section: Resultsmentioning

confidence: 99%

“…The phagocytic index was measured as described previously [7], [14]. FITC-conjugated E. coli and fluorescent beads were added to peritoneal macrophages or RAW 264.7 cells at a ratio of 2:1 for 20 min and 30 min, respectively, at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…The phagocytic index was quantified by flow cytometry [7], [14]. Rb1 (0 or 5 mg/kg) was injected intraperitoneally into mice.…”

Section: Methodsmentioning

confidence: 99%

“…The binding of pathogens or specific molecules by these receptors results in the rapid responses of a series of intracellular signaling proteins, including the Rho family of G proteins, which play an important role in the reorganization of the actin cytoskeleton [1], [3]. Recent studies have reported that several kinases including p38 mitogen-activated protein kinase (MAPK) or adenosine monophosphate-activated protein kinase can activate Rac1, a subfamily of the Rho family, which plays a pivotal role in the phagocytic uptake of particles [5], [6], [7], [8].…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have revealed that the activation of p38 MAPK can regulate actin cytoskeletal reorganization, which plays an important role in phagocytosis, cell migration, and morphological changes in various cell populations [9], [10], [11]. Specifically, p38 MAPK activation by various stimuli enhances the ability of macrophages to phagocytose bacteria [7], [11], [12], [13], [14]. Stimulation of toll-like receptors (TLRs) with specific ligands enhances bacterial phagocytosis by macrophages and was blocked by p38 MAPK inhibitors or small-interfering RNA (siRNA)–mediated knockdown of p38 MAPK [11], [13].…”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside Rb1 increases macrophage phagocytosis through p38 mitogen-activated protein kinase/Akt pathway

Xin

Quan

Kim

et al. 2019

Journal of Ginseng Research

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Background Ginsenoside Rb1, a triterpene saponin, is derived from the Panax ginseng root and has potent antiinflammatory activity. In this study, we determined if Rb1 can increase macrophage phagocytosis and elucidated the underlying mechanisms. Methods To measure macrophage phagocytosis, mouse peritoneal macrophages or RAW 264.7 cells were cultured with fluorescein isothiocyanate–conjugated Escherichia coli , and the phagocytic index was determined by flow cytometry. Western blot analyses were performed. Results Ginsenoside Rb1 increased macrophage phagocytosis and phosphorylation of p38 mitogen-activated protein kinase (MAPK), but inhibition of p38 MAPK activity with SB203580 decreased the phagocytic ability of macrophages. Rb1 also increased Akt phosphorylation, which was suppressed by LY294002, a phosphoinositide 3-kinase inhibitor. Rb1-induced Akt phosphorylation was inhibited by SB203580, (5Z)-7-oxozeaenol, and small-interfering RNA (siRNA)–mediated knockdown of p38α MAPK in macrophages. However, Rb1-induced p38 MAPK phosphorylation was not blocked by LY294002 or siRNA-mediated knockdown of Akt. The inhibition of Akt activation with siRNA or LY294002 also inhibited the Rb1-induced increase in phagocytosis. Rb1 increased macrophage phagocytosis of IgG-opsonized beads but not unopsonized beads. The phosphorylation of p21 activated kinase 1/2 and actin polymerization induced by IgG-opsonized beads and Rb1 were inhibited by SB203580 and LY294002. Intraperitoneal injection of Rb1 increased phosphorylation of p38 MAPK and Akt and the phagocytosis of bacteria in bronchoalveolar cells. Conclusion These results suggest that ginsenoside Rb1 enhances the phagocytic capacity of macrophages for bacteria via activation of the p38/Akt pathway. Rb1 may be a useful pharmacological adjuvant for the treatment of bacterial infections in clinically relevant conditions.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…The phagocytic index was quantified by flow cytometry [7], [14]. Rb1 (0 or 5 mg/kg) was injected intraperitoneally into mice.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Ginsenoside Rb1 increases macrophage phagocytosis through p38 mitogen-activated protein kinase/Akt pathway

Xin

Quan

Kim

et al. 2019

Journal of Ginseng Research

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RETRACTED ARTICLE: Lysophosphatidylcholine induces adenosine release from macrophages via TRPM7-mediated mitochondrial activation

Youssef

Song

2022

Purinergic Signalling

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Impact of the immune response modification by lysophosphatidylcholine in the efficacy of antibiotic therapy of experimental models of peritoneal sepsis and pneumonia by Pseudomonas aeruginosa: LPC therapeutic effect in combined therapy

Parra-Millán

Ayerbe-Algaba

et al. 2022

Enfermedades Infecciosas y Microbiología Clínica

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Immune response stimulation may be an adjuvant to antimicrobial treatment. Here, we evaluated the impact of immune response modification by lysophosphatidylcholine (LPC) combined with imipenem or ceftazidime in murine models of peritoneal sepsis (PS) and pneumonia by Pseudomonas aeruginosa. Imipenem and ceftazidime-susceptible strain (Pa39), and imipenem and ceftazidime-resistant strain (Pa238) were used. Ceftazidime pharmacokinetic and pharmacodynamic parameters were determined. Therapeutic efficacy, and TNF-α and IL-10 levels were determined in murine models of PS and pneumonia by Pa39 and Pa238 treated with LPC, imipenem or ceftazidime, alone or in combination. In PS model, LPC+ceftazidime reduced spleen and lungs Pa238 concentrations (-3.45 and -3.56 log10 CFU/g; P<0.05) than ceftazidime monotherapy, while LPC+imipenem maintained the imipenem efficacy (-1.66 and -1.45 log10 CFU/g; P>0.05). In pneumonia model, LPC+ceftazidime or LPC+imipenem reduced lungs Pa238 concentrations (-2.37 log10 CFU/g, P=0.1, or -1.35 log10 CFU/g, P=0.75). For Pa39 no statistically significant difference has been observed in PS and pneumonia models between combined therapy and monotherapy. Moreover, LPC+imipenem and LPC+ceftazidime decreased and increased significantly TNF-α and IL-10 levels, respectively, in comparison with untreated controls and monotherapies. These results demonstrate the impact of immune response modification by LPC plus antibiotics on the prognosis of infections by ceftazidime-resistant P. aeruginosa.

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Stearoyl lysophosphatidylcholine enhances the phagocytic ability of macrophages through the AMP-activated protein kinase/p38 mitogen activated protein kinase pathway

Cited by 15 publications

References 46 publications

Ginsenoside Rb1 increases macrophage phagocytosis through p38 mitogen-activated protein kinase/Akt pathway

Ginsenoside Rb1 increases macrophage phagocytosis through p38 mitogen-activated protein kinase/Akt pathway

RETRACTED ARTICLE: Lysophosphatidylcholine induces adenosine release from macrophages via TRPM7-mediated mitochondrial activation

Impact of the immune response modification by lysophosphatidylcholine in the efficacy of antibiotic therapy of experimental models of peritoneal sepsis and pneumonia by Pseudomonas aeruginosa: LPC therapeutic effect in combined therapy

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