• Title/Summary/Keyword: phagocytosis

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The Effects of Ginseng Components on the Signal Transduction in the Activation of Murine Macrophages (생쥐 대식세포의 활성시 신호전달에 미치는 인삼성분들의 영향)

  • 신은경;박한우
    • Journal of Ginseng Research
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    • v.20 no.2
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    • pp.159-167
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    • 1996
  • To study the effects of ginseng saponin components on the signal transduction in the ac tivation of murine macrophages, phagocytosis and Intracellular calcium concentration of peritoneal exuded mouse macrophages were examined. The phagocytosis was increased significantly after treatment with total saponin, diol-saponin, $Rg_1$ and $Rg_2$, but triol-saponin was unable to increase phagocytosis. The phagocytosis were increased when H7, a PKC inhibitor, was pretreated and increased significantly by saponin fractions except total saponin. Pertussis toxin, which inactivates G-protein, decreased the phagocytosis. But the phagocytosis was restored to the control level by saponin fractions and the phagocytosis was increased significantly by $Rg_2$ and $Rg_2$. The triol saponin increased phagocytosis approximately by 2-fold as compared with the TMB-8 treated group. Peritoneal exuded macrophages displayed a prominent rise in cytosolic calcium following treatment with triol-saponin, $Rg_1$, $Rg_2$ and $Rg_2$. Incubation of macrophages with PT resulted in an inhibition of cytosolic calcium mobilization, but increased cytosolic calcium mobilization with saponin fraction.

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Effects of Rudbeckia laciniata Extract on Phagocytosis of Serum-Opsonized Zymosan Particles in Macrophages (대식세포의 혈청으로 식균된 자이모잔의 탐식능에 대한 삼잎국화 추출물의 효과)

  • Kim, Jun-Sub
    • The Korean Journal of Food And Nutrition
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    • v.29 no.3
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    • pp.341-346
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    • 2016
  • Phagocytosis is a primary and an essential step of host defense, and is triggered by the interaction of particles with specific receptor of macrophages. In this study, we investigated the effect of extracts of Rudbeckia laciniata (RLE) on the phagocytic activity of macrophage, by monitoring the phagocytosis-associated signal transduction. RLE markedly increased phagocytosis of serum-opsonized zymosan particles (SOZ), while phagocytosis of IgG-opsonized zymosan particles (IOZ) or none-opsonized zymosan particles (NOZ) remained unaffected. However, RLE did not affect the binding of opsonized zymosan particles (OZ) with the cell surface of macrophage. This suggests that RLE may regulate SOZ-induced intracellular signaling during phagocytosis of macrophage. To confirm this hypothesis, we investigated whether RLE was involved in the RhoA-mediated signal transduction during phagocytosis of SOZ. Inhibitors of the RhoA-mediated signaling pathway, such as Y-27632 (for ROCK), ML-7 (for MLCK), and Tat-C3 (for RhoA), totally blocked phagocytosis of SOZ enhanced by RLE, as well as phagocytosis of SOZ. Additionally, RhoA activity was markedly increased when cells were treated with RLE, suggesting that RLE could increase the phagocytic activity of macrophage via RhoA-ROCK/MLCK signal pathway. Thus, RLE may be used to develop functional foods for immunity.

Effect of Inositol-phosphatase on Fc Receptor-mediated Phagocytosis of Macrophages (대식세포의 Fc 수용체를 통한 탐식에 미치는 Inositol-phosphatase의 영향)

  • Kim, Jong-Hyun
    • IMMUNE NETWORK
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    • v.5 no.3
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    • pp.144-149
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    • 2005
  • Background: Fc receptor-mediated phagocytosis is a complex process involving the activation of kinases and phosphatases. FcgammaRIIB has been known to transduces inhibitory signals through an immunoreceptor tyrosine-based inhibitory motif (ITIM) in cytoplasmic domains. In this study, we examined the involvement of inositol-phosphatase in the Fc receptor-mediated phagocytosis. Methods: J774 cells were infected using vaccinia viral vector containing SH2 domain-containing inositol-phosphatase (SHIP) cDNA and stimulated with the sensitized sheep red blood cells. Results: Stimulation of J774 cells induced the tyrosine phosphorylation of SHIP which was maximal at 5 minutes. Phosphatidylinositol-3 (PI-3) kinase inhibitor (wortmannin) inhibits J774 cell phagocytosis of sensitized sheep red blood cells in a dose-dependent manner. Heterologious expression of SHIP in J774 cells inhibits phagocytosis of sensitized sheep red blood cells in a dose-dependency manner, but catalytically dead mutants of SHIP has no effect on phagocytosis. Conclusion: These results strongly suggest that the active signals mediated by PI-3 kinase are opposed by inhibitory signals through SHIP in the regulation of Fc receptor-mediated phagocytosis.

Effect of Various Agents on Oral Bacterial Phagocytosis in THP-1 Cells

  • Song, Yuri;Lee, Hyun Ah;Na, Hee Sam;Jin, Chung
    • International Journal of Oral Biology
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    • v.43 no.4
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    • pp.217-222
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    • 2018
  • Phagocytosis is a fundamental process in which phagocytes capture and ingest foreign particles including pathogenic bacteria. Several oral pathogens have anti-phagocytic strategies, which allow them to escape from and survive in phagocytes. Impaired bacteria phagocytosis increases inflammation and contributes to inflammatory diseases. The purpose of this study is to investigate the influences of various agents on oral pathogenic phagocytosis. To determine phagocytosis, Streptococcus mutans, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis were stained with 5-(and-6)-carboxyfluorescein diacetate succinimidyl ester (CFSE), and was measured using flowcytometery and confocal microscopy. The influencing factors on phagocytosis were evaluated through the pretreatment of ROS inhibitor (N-acetyl-L-cysteine (NAC)), lysozyme, potassium chloride (KCI) and adenosine triphosphate (ATP) in THP-1 cells. Expression of pro-inflammatory cytokines was determined by enzyme-linked immunosorbent assay (ELISA). The phagocytosis of various bacteria increased in a MOI-dependent manner. Among the tested bacteria, phagocytosis of P. gingivalis showed the highest fluorescent intensity at same infection time. Among the tested inhibitors, the NAC treatment significantly inhibited phagocytosis in all tested bacteria. In addition, NAC treatment indicated a similar pattern under the confocal microscopy. Moreover, NAC treatment significantly increased the bacteria-induced secretion of $IL-1{\beta}$ among the tested inhibitors. Taken together, we conclude that the phagocytosis occurs differently depending on each bacterium. Down-regulation by ROS production inhibited phagocytosis and lead increased of oral pathogens-associated inflammation.

Phagocytic Roles of Glial Cells in Healthy and Diseased Brains

  • Jung, Yeon-Joo;Chung, Won-Suk
    • Biomolecules & Therapeutics
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    • v.26 no.4
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    • pp.350-357
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    • 2018
  • Glial cells are receiving much attention since they have been recognized as important regulators of many aspects of brain function and disease. Recent evidence has revealed that two different glial cells, astrocytes and microglia, control synapse elimination under normal and pathological conditions via phagocytosis. Astrocytes use the MEGF10 and MERTK phagocytic pathways, and microglia use the classical complement pathway to recognize and eliminate unwanted synapses. Notably, glial phagocytosis also contributes to the clearance of disease-specific protein aggregates, such as ${\beta}$-amyloid, huntingtin, and ${\alpha}$-synuclein. Here we reivew recent findings showing that glial cells are active regulators in brain functions through phagocytosis and that changes in glial phagocytosis contribute to the pathogenesis of various neurodegenerative diseases. A better understanding of the cellular and molecular mechanisms of glial phagocytosis in healthy and diseased brains will greatly improve our current approach in treating these diseases.

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

  • Xin, Chun;Quan, Hui;Kim, Joung-Min;Hur, Young-Hoe;Shin, Jae-Yun;Bae, Hong-Beom;Choi, Jeong-Il
    • Journal of Ginseng Research
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    • v.43 no.3
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    • pp.394-401
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    • 2019
  • 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 mitogenactivated 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 $p38{\alpha}$ 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.

Enhancement of Type A Macrophage Scavenger Receptor Expression by Ginsenoside Rg3 in Rat Microglia (흰쥐 뇌 소교세포에서 진세노사이드 Rg3의 Type A Macrophage Scavenger Receptor 발현 증진효과)

  • Joo, Seong-Soo;Hwang, Kwang-Woo;Lee, Do-Ik
    • YAKHAK HOEJI
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    • v.49 no.2
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    • pp.147-150
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    • 2005
  • Macrophage scavenger receptors (MSRs) induce microglial interaction with ${\beta}$-amyloid fibrils (fA${\beta}$) that are associated with Alzheimer's disease (AD). Although microglia are know n to have a dual effect on formation of plaque and clearance of fA${\beta}$ in the AD brain, receptor-mediated phagocytosis is a very important tool for preventing amyloid plaque via activated microglia in the early stage of AD. In the study, we examined whether ginsonoside Rg3 enhances the microglial Phagocytosis of A${\beta}$1-42 through Phagocytosis assay, gene expression (RT-PCR) and protein assay (western blots) for the cell responsiveness presented between Rg3-treated and non-treated groups. Fluro-labeled Ac-LDL and E.coli particles were used as control proteins for phagocytosis. In previous studies, this was a particularly interesting property of Rg3 in the stimulation and phagocytosis of macrophages in the periphery. We report here that ginsenoside Rg3 increased the expression of type-A MSR (MSR-A) in microglia and thus accelerated the phagocytosis with an effective degradation of engulfed fA${\beta}$. This result suggests that Rg3 may play an important role in removing fA${\beta}$ by enhancing the receptor-mediated phagocytosis. In addition, Rg3 could be a potential candidate for balancing the rate of production of fA${\beta}$ in AD brain.

Detection of Phagocytosis-Promoting Factor of Culture Supernatant from Feline Peripheral Blood Mononuclear Cells Cultured with Egg White Derivatives (계난백유래물질로 배양한 고양이 말초혈액 단핵구세포 배양상층액중의 탐식촉진인자 검출)

  • 양만표;김기홍
    • Journal of Veterinary Clinics
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    • v.16 no.1
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    • pp.31-36
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    • 1999
  • The aim of this study is to determine the phagocytosis-promoting factor(s) for feline peripheral blood polymorphonuclear cells (PMN) by culture supernatant from mono-nuclear cells (MNC) treated with egg white derivatives (EWD). The phagocytic activity of PMN was analyzed by a flow cytometry system. The EWD did not show direct effect on the phagocytic response of PMN. The phagocytic activity of PMN was enhanced by culture supernatant from MNC but not PMN treated with EWD. Therefore, it was suggested that the enhanced phagocytic activity of feline PMN could be mediated by humoral factor(s) released from MNC treated with EWD. Thus, the phagocytosis-promoting factor(s) in supernatant fraction from MNC culture treated with EWD were isolated by reverse phase high pressure liquid chromatography. The resulting supernatant fraction on 29.02 minutes of retention time showed high phagocytic activity of PMN. The molecular weight of this supernatant fraction was 16 to 18 kDa when analyzed by capillary electrophoresis. The isoelectric point was pH 5.76 when assessed by ion-exchange chromatography. These results suggest that EWD stimulates feline MNC to elaborate a phagocytosis-promoting factor, 16 to 18 kDa of molecular weight, which could be an important mediator for the enhancement of phagocytic activity of feline peripheral blood phagocytes. Further study will be needed to elucidate this phagocytic factor.

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Effect of White Ginseng on the Function of Mouse Peritoneal Macrophages and their Gene Expression (백삼성분이 마우스 복강 탐식세포의 기능 및 유전자 발현에 미치는 영향)

  • 배지현
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.26 no.6
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    • pp.1252-1257
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    • 1997
  • In order to investigate the immunomodulatory mechanism of white ginseng, the effects of total saponin of Ginsenoside Rb$_2$component on the phagocytosis and reactive oxygen intermediate(ROI) production of mouse peritoneal macrophages were studied. Both phagocytosis assay nitrobluetetrazolium reduction test showed 20$\mu\textrm{g}$/ml concentration of total saponin significantly increased the activity of phagocytosis and production of ROI. Also cytokine gene expression of the macrophages was analyzed using reverse transcription polymerase chain reaction. In the RT-PCR assay, 20$\mu\textrm{g}$/ml concentration of either total saponin or Ginsenoside Rb$_2$increased IL-1 and TNF expression of the macrophages.

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Polymorphonuclear Neutrophil Dysfunctions in Streptozotocin-induced Type 1 Diabetic Rats

  • Nabi, A.H.M. Nurun;Islam, Laila N.;Rahman, Mohanmmad Mahfuzur;Biswas, Kazal Boron
    • BMB Reports
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    • v.38 no.6
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    • pp.661-667
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    • 2005
  • Since conflicting results have been reported on non-specific immune response in type 1 diabetes, this study evaluates polymorphonuclear neutrophil (PMN) functions in the infection free Long Evan diabetic rats (type 1) by using tests that include: polarization assay, phagocytosis of baker's yeasts (Saccharomyces cerevisiae) and nitroblue tetrazolium (NBT) dye reduction. Polarization assay showed that neutrophils from diabetic rats were significantly activated at the basal level compared to those from the controls (p < 0.001). After PMN activation with N-formyl-methionyl-leucyl-phenylalanine (FMLP), control neutrophils were found to be more polarized than those of the diabetic neutrophils and the highest proportions of polarization were found to be 67% and 57% at $10^{-7}\;M$ FMLP, respectively. In the resting state, neutrophils from the diabetic rats reduced significantly more NBT dye than that of the controls (p < 0.001). The percentages of phagocytosis of opsonized yeast cells by the neutrophils from control and diabetic rats were 87% and 61%, respectively and the difference was statistically significant (p < 0.001). Evaluation of the phagocytic efficiency of PMNs revealed that control neutrophils could phagocytose $381{\pm}17$ whereas those from the diabetic rats phagocytosed $282{\pm}16$ yeast cells, and the efficiency of phagocytosis varied significantly (p < 0.001). Further, both the percentages of phagocytosis and the efficiency of phagocytosis by the diabetic neutrophils were inversely related with the levels of their corresponding plasma glucose (p = 0.02; r = -0.498 and p < 0.05; r = -0.43, respectively), which indicated that increased plasma glucose reduced the phagocytic ability of neutrophils. Such relationship was not observed with the control neutrophils. These data clearly indicate that PMN functions are altered in the streptozotocin (STZ) - induced diabetic rats, and hyperglycemia may be the cause for the impairment of their functions leading to many infectious episodes.