Extraction, Characterization and Immunological Activity of Polysaccharides from Cynomorium songaricum Rupr.

2021 ◽  
Vol 11 (8) ◽  
pp. 1543-1554
Author(s):  
Min Li ◽  
Jianhua Yang ◽  
Junping Hu
Keyword(s):  
Inflammatory Cytokines ◽  
Phagocytic Activity ◽  
Active Component ◽  
Immunomodulatory Activity ◽  
Immunological Activity ◽  
Raw264.7 Macrophages ◽  
Immunosuppressed Mice

Cynomorium songaricum Rupr. (CSP) have been used widely in TCM for many years, polysaccharides from CSP are main active component. In our previous research, we found that CSP play a role of immunomodulatory activity in vitro, but its mechanisms and in vivo immunomodulatory activity hadn’t been explored. In present study, we firstly extracted CSP and identified two new fractions CSP-a, CSP-b. To assess the immunomodulatory activity of CSP in vivo, cyclophosphamide (CTX)-induced immunosuppressed mice models were generated and then treated with CSP. The results demonstrated that CSP could improve thymus and spleen indices, phagocytic and clearance index, serum hemolysin, inflammatory cytokines productions in serum. To explore the mechanisms of CSP, CSP-a, CSP-b, RAW264.7 macrophages were used to evaluate the immunomodulatory activity in vitro, the results demonstrated that CSP, CSP-a, CSP-b can induce macrophage proliferation, enhance the phagocytic activity and increase cytokines expression. CSP, CSP-a, CSP-b possessed the immunomodulatory activity by inducing the phosphorylation of MAPKs. This study suggested that CSP may be useful for lessening chemotherapy-induced immunosuppression and proposed the basis for the clinical application of CSP.

scholarly journals HDAC2 attenuates airway inflammation by suppressing IL-17A production in HDM-challenged mice

2019 ◽  
Vol 316 (1) ◽  
pp. L269-L279 ◽  
Author(s):  
Tianwen Lai ◽  
Mindan Wu ◽  
Chao Zhang ◽  
Luanqing Che ◽  
Feng Xu ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Protective Role ◽  
In Vivo Models

Histone deacetylase (HDAC)2 is expressed in airway epithelium and plays a pivotal role in inflammatory cells. However, the role of HDAC2 in allergic airway inflammation remains poorly understood. In the present study, we determined the role of HDAC2 in airway inflammation using in vivo models of house dust mite (HDM)-induced allergic inflammation and in vitro cultures of human bronchial epithelial (HBE) cells exposed to HDM, IL-17A, or both. We observed that HDM-challenged Hdac2+/− mice exhibited substantially enhanced infiltration of inflammatory cells. Higher levels of T helper 2 cytokines and IL-17A expression were found in lung tissues of HDM-challenged Hdac2+/− mice. Interestingly, IL-17A deletion or anti-IL-17A treatment reversed the enhanced airway inflammation induced by HDAC2 impairment. In vitro, HDM and IL-17A synergistically decreased HDAC2 expression in HBE cells. HDAC2 gene silencing further enhanced HDM- and/or IL-17A-induced inflammatory cytokines in HBE cells. HDAC2 overexpresion or blocking IL-17A gene expression restored the enhanced inflammatory cytokines. Collectively, these results support a protective role of HDAC2 in HDM-induced airway inflammation by suppressing IL-17A production and might suggest that activation of HDAC2 and/or inhibition of IL-17A production could prevent the development of allergic airway inflammation.

scholarly journals Immunomodulatory Activities of Dendrophthoe falcata (L.f) Ettingsh in Experimental Animals: In vitro and In vivo Investigations

2011 ◽  
Vol 3 (3) ◽  
pp. 619-630 ◽  
Author(s):  
S. P. Pattanayak ◽  
P. M. Mazumder
Keyword(s):  
Antibody Titer ◽  
Phagocytic Activity ◽  
Reticuloendothelial System ◽  
Peritoneal Macrophages ◽  
Immunomodulatory Activity ◽  
Hydroalcoholic Extract ◽  
Dendrophthoe Falcata ◽  
Stimulation Of

In the present study, an attempt was made to screen immunomodulatory activity of the hydroalcoholic extract (HEDF) of Dendrophthoe falcata (L.f.) Ettingsh (Loranthaceae), an Indian Ayurvedic plant, on different arms of the immune system. HEDF was evaluated for immunological function by studying delayed type hypersensitivity (DTH) to sheep RBCs, nitric oxide (NO) release from murine peritoneal macrophages, phagocytic activity of polymorphonuclear (PMN) cells in vitro and reticuloendothelial system in vivo, plaque forming cell response of splenic lymphocytes to sheep erythrocytes, haemagglutination antibody titer and neutrophil adhesion test. Significant increase in NO production by mouse peritoneal macrophages was detected in culture supernatants indicated increased phagocytic activity of macrophages. After post oral administration of HEDF in three doses of 250, 475 and 950 mg/kg body weight, a significant increase in phagocytic activity of PMN cells/reticuloendothelial system, stimulation of neutrophil function and splenic antibody secreting cells, were also noticed. Stimulation of humoral immune response was further observed with elevation in haemagglutination antibody titer. Heightened DTH reaction suggested convincing evidence for activation of cellular immune system. Present study thus confirms the immunomodulatory activity of the hydroalcoholic extract of D. falcata and the immunomodulatory responses were found to be dose dependent manner.Keywords: Dendrophthoe falcata; Antibody titer; Neutrophil adhesion; Phagocytic activity.© 2011 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved.doi:10.3329/jsr.v3i3.7655               J. Sci. Res. 3 (3), 629-640 (2011)

Enhanced β-Catenin/Foxo1 Activity Alleviates Pulmonary Fibrosis by Inhibiting β-Catenin/T Cell Factor Signaling

2020 ◽  
Vol 10 (2) ◽  
pp. 182-188
Author(s):  
Kun Gui ◽  
Yu Huang ◽  
Meijin Wang ◽  
Jun Yang
Keyword(s):  
Extracellular Matrix ◽  
Pulmonary Fibrosis ◽  
Inflammatory Cytokines ◽  
Underlying Mechanism ◽  
Control Group ◽  
Kidney Fibrosis ◽  
Mrc5 Cell

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrosing interstitial pneumonia, resulting in chronic respiratoryfailure and eventually death. β-catenin/Foxo1 showed a protective property in kidney fibrosis, but the role of β-catenin/Foxo1 in IPF was unclear. Our study aimed to investigate the role of β-catenin/Foxo1 in IPF and explore its underlying mechanism. The IPF model was established by injection of bleomycin (BLM) in vivo and stimulation by TGF-β1 in MRC5 cell in vitro. Haematoxylin-eosin staining and Masson’s trichrome staining were performed to examine histopathological injury in lung. Protein expression of corresponding genes was detected using western blot. Immunofluorescence staining assay was carried out to detect the expression of β-catenin, Foxo1, TCF and α-SMA. The expression levels of inflammatory cytokines were determined using ELISA kit assay. The results showed that BLM induced a serious pulmonary injury and proliferated fibroblasts. A higher interaction of β-catenin with TCF and a lower interaction of β-catenin with Foxo1 was found in BLM group compared to the control group. TGF-β1 promoted β-catenin/TCF, whereas ICG-001 inhibited β-catenin/TCF, and promoted β-catenin/Foxo1. Furthermore, ICG-001 reversed TGF-β1 induced largely production of inflammatory cytokines and accumulation of extracellular matrix, as well as high expression of α-SMA. However, AS1842856, a FOXO1 antagonist, strengthened the effects induced by TGF-β1. In summary, our study revealed that β-catenin/Foxo1 protected against IPF through inhibiting inflammatory response and extracellular matrix accumulation, providing an alternative approach to explain the potential mechanism of IPF and seek for more effective therapeutic drugs.

scholarly journals MicroRNA-181a-5p regulates inflammatory response of macrophages in sepsis

Open Medicine ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. 899-908 ◽  
Author(s):  
Zheng Huang ◽  
Hang Xu
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Sirtuin 1 ◽  
Raw 264.7 Cells ◽  
Inflammatory Factors ◽  
Raw 264.7 ◽  
Raw264.7 Macrophages ◽  
Pathway Activation

AbstractThe aim of this study was to evaluate the role of miR-181a-5p in sepsis, and to further explore the molecular mechanism. RAW 264.7 cells were stimulated with 1 μg/ml LPS for 4 hours. Firstly, qRT-PCR and ELISA was adopted to evaluate the expression of miR-181a-5p and p ro-inflammatory cytokines in RAW 264.7 macrophages a fter LPS stimulation. Results showed that pro-inflammatory cytokines and miR-181a-5p were significantly increased after LPS treatment. Then, we identified that sirtuin-1 (SIRT1) was a direct target of miR-181a-5p and it was down-regulated in LPS treated RAW264.7 macrophages. Furthermore, the data suggested that the miR-181a-5p inhibitor significantly inhibited LPS enhanced inflammatory cytokines expression and NF-κB pathway activation, and these changes were eliminated by SIRT1 silencing. Moreover, the role of the miR-181a-5p inhibitor on sepsis was studied in vivo. We found that the miR-181a-5p inhibitor significantly decreased the secretion of inflammatory factors, and the levels of creatine (Cr), blood urea nitrogen (BUN), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in a serum for mice with sepsis. However, all the effects were reversed by SIRT1-siRNA. In summary, these results indicated that miR-181a-5p was involved in sepsis through regulating the inflammatory response by targeting SIRT1, suggesting that miR-181a-5p may be a potential target for the treatment of sepsis.

scholarly journals Immunomodulatory and Antimicrobial Activity of Babassu Mesocarp Improves the Survival in Lethal Sepsis

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Elizabeth S. B. Barroqueiro ◽  
Dayanna S. Prado ◽  
Priscila S. Barcellos ◽  
Tonicley A. Silva ◽  
Wanderson S. Pereira ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antimicrobial Activity ◽  
Phenolic Acids ◽  
Cecal Ligation ◽  
Significant Inhibition ◽  
Lymphoid Cells ◽  
Immunomodulatory Activity ◽  
Immunological Activity

Attalea speciosasynOrbignya phalerataMart. (babassu) has been used in the treatment of inflammatory and infectious diseases.Aim of the study. To investigate the antimicrobial and immunological activity of babassu mesocarp extract (EE).Material and Methods.Thein vitroantimicrobial activity was evaluated by disk diffusion assay and by determination of the minimum inhibitory concentration (MIC) toEscherichia coli,Pseudomonas aeruginosa,Enterococcus faecalis,Staphylococcus aureus,and methicillin-resistantStaphylococcus aureus(MRSA). The flavonoids and phenolic acids content were determined by chromatography. Thein vivoassays were performed in Swiss mice submitted to sepsis by cecal ligation and puncture (CLP). The mice received EE subcutaneously (125 or 250 mg/Kg), 6 hours after the CLP. The number of lymphoid cells was quantified and the cytokines production was determined by ELISA after 12 h.Results.EE was effective as antimicrobial toE. faecalis,S. aureus, and MRSA. EE is rich in phenolic acids, a class of compounds with antimicrobial and immunological activity. An increased survival can be observed in those groups, possibly due to a significant inhibition of TNF-αand IL-6.Conclusions.The EE showed specific antimicrobial activityin vitroand an important antiseptic effectin vivopossibly due to the antimicrobial and immunomodulatory activity.

scholarly journals Role of Muramyl Dipeptide in Lipopolysaccharide-Mediated Biological Activity and Osteoclast Activity

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Hideki Kitaura ◽  
Masahiko Ishida ◽  
Keisuke Kimura ◽  
Haruki Sugisawa ◽  
Akiko Kishikawa ◽  
...  
Keyword(s):  
Biological Activities ◽  
Muramyl Dipeptide ◽  
Mapk Signaling ◽  
Osteoclast Formation ◽  
Mitogen Activated Protein Kinase ◽  
Immunological Activity ◽  
Mitogen Activated Protein

Lipopolysaccharide (LPS) is an endotoxin and bacterial cell wall component that is capable of inducing inflammation and immunological activity. Muramyl dipeptide (MDP), the minimal essential structural unit responsible for the immunological activity of peptidoglycans, is another inflammation-inducing molecule that is ubiquitously expressed by bacteria. Several studies have shown that inflammation-related biological activities were synergistically induced by interactions between LPS and MDP. MDP synergistically enhances production of proinflammatory cytokines that are induced by LPS exposure. Injection of MDP induces lethal shock in mice challenged with LPS. LPS also induces osteoclast formation and pathological bone resorption; MDP enhances LPS induction of both processes. Furthermore, MDP enhances the LPS-induced receptor activator of NF-κB ligand (RANKL) expression and toll-like receptor 4 (TLR4) expression bothin vivoandin vitro. Additionally, MDP enhances LPS-induced mitogen-activated protein kinase (MAPK) signaling in stromal cells. Taken together, these findings suggest that MDP plays an important role in LPS-induced biological activities. This review discusses the role of MDP in LPS-mediated biological activities, primarily in relation to osteoclastogenesis.

scholarly journals Pleural Mesothelial Cells Modulate the Inflammatory/Profibrotic Response During SARS-CoV-2 Infection

2021 ◽  
Vol 8 ◽  
Author(s):  
Giulia Matusali ◽  
Flavia Trionfetti ◽  
Veronica Bordoni ◽  
Roberta Nardacci ◽  
Laura Falasca ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Wilms Tumor ◽  
Mesothelial Cells ◽  
Membrane Receptors ◽  
Productive Infection ◽  
Rt Pcr ◽  
Plasma Membrane Receptors

Although lung fibrosis has a major impact in COVID-19 disease, its pathogenesis is incompletely understood. In particular, no direct evidence of pleura implication in COVID-19-related fibrotic damage has been reported so far. In this study, the expression of epithelial cytokeratins and Wilms tumor 1 (WT1), specific markers of mesothelial cells (MCs), was analyzed in COVID-19 and unrelated pleura autoptic samples. SARS-CoV-2 replication was analyzed by RT-PCR and confocal microscopy in MeT5A, a pleura MC line. SARS-CoV-2 receptors were analyzed by RT-PCR and western blot. Inflammatory cytokines from the supernatants of SARS-CoV-2-infected MeT5A cells were analysed by Luminex and ELLA assays. Immunohistochemistry of COVID-19 pleura patients highlighted disruption of pleura monolayer and fibrosis of the sub-mesothelial stroma, with the presence of MCs with fibroblastoid morphology in the sub-mesothelial stroma, but no evidence of direct infection in vivo. Interestingly, we found evidence of ACE2 expression in MCs from pleura of COVID-19 patients. In vitro analysis shown that MeT5A cells expressed ACE2, TMPRSS2, ADAM17 and NRP1, plasma membrane receptors implicated in SARS-CoV-2 cell entry and infectivity. Moreover, MeT5A cells sustained SARS-CoV-2 replication and productive infection. Infected MeT5A cells produced interferons, inflammatory cytokines and metalloproteases. Overall, our data highlight the potential role of pleura MCs as promoters of the fibrotic reaction and regulators of the immune response upon SARS-CoV-2 infection.

Neutrophil-Derived Exosomes Induce M1 Macrophage Polarization and Prime Macrophage Pyroptosis via miR-30d-5p in Sepsis

2021 ◽  
Author(s):  
Yang Jiao ◽  
Ti Zhang ◽  
Chengmi Zhang ◽  
Haiying Ji ◽  
Xingyu Tong ◽  
...  
Keyword(s):  
Macrophage Activation ◽  
Macrophage Polarization ◽  
Cecal Ligation ◽  
Polymorphonuclear Neutrophils ◽  
Raw264.7 Macrophages ◽  
M1 Macrophage ◽  
Tnf Α

Abstract Background: Polymorphonuclear neutrophils (PMNs) have been demonstrated to play a role in proinflammatory M1 activation and macrophage (Mϕ) pyroptosis in sepsis. Accumulating evidence suggests PMN-derived exosomes as a new subcellular entity acting as a fundamental link between PMN-driven inflammation and tissue damage. However, the role of PMN-derived exosomes in sepsis remains unclear. This study aimed to determine whether PMN-derived exosomes play a role in proinflammatory M1 activation and Mϕ pyroptosis in sepsis and explore the potential mechanisms involved. Methods: Exosomes were isolated from the supernatant of PMNs activated with phosphate buffered saline (PBS) or tumor necrosis factor (TNF)-α, cocultured with Raw264.7 macrophages or BMDMs, and then assayed for macrophage polarization and pyroptosis. To examine the role of exosomes in vivo, PMN-derived exosomes were administered to mice, and then examined for lung inflammation. Results: After activated by TNF-α, PMNs released exosomes (TNF-Exo) to promote M1 macrophage activation both in vivo and in vitro. In addition, TNF-Exo primed macrophages for pyroptosis by upregulating NLRP3 inflammasome expression through NF-κB signaling pathway. Mechanistic studies demonstrated that miR-30d-5p mediated the function of TNF-Exo by targeting SOCS-1 and SIRT1 in macrophages. Furthermore, treatment of miR-30d-5p inhibitors in vivo significantly decreased cecal ligation and puncture (CLP) or TNF-Exo-induced M1 macrophage activation and macrophage death in the lung. Lung injury was also alleviated by miR-30d-5p inhibitors.Conclusions: In this study, we identified a novel mechanism of PMN-Mϕ interaction in sepsis, demonstrating that exosomal miR-30d-5p from PMNs induced M1 macrophage polarization and primed Mϕ for pyroptosis by activating NF-κB signaling. These findings suggest a previously unidentified role of neutrophil-derived exosomes in sepsis and may lead to new therapeutic approaches.

scholarly journals Attenuating Immune Response of Macrophage by Enhancing Hydrophilicity of Ti Surface

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Xiaohan Dai ◽  
Yan Wei ◽  
Xuehui Zhang ◽  
Song Meng ◽  
Xiaoju Mo ◽  
...  
Keyword(s):  
Immune Response ◽  
Cell Formation ◽  
Underlying Mechanism ◽  
Immunomodulatory Activity ◽  
Inflammatory Factor ◽  
Surface Hydrophilicity ◽  
Raw264.7 Macrophages ◽  
Assay Result

Immune responses can determine thein vivofate of implanted materials. The strategy for developing implants has shifted towards using materials with immunomodulatory activity. However, the immunoregulatory effect of hydrophilicity of titanium surface on the macrophage behavior and its underlying mechanism remain poorly understood. Here, the Ti surface hydrophilicity-dependent behavior of murine RAW264.7 macrophages was investigatedin vitro. Two laboratory models with significantly different surface hydrophilicity and similar roughness were established with Ti-polished and Ti-H2O2surfaces. The results of cell morphology observation showed that the Ti-H2O2surface yielded enhanced cell adhesion and less multinucleated cell formation. CCK-8 assay indicated that the growth rate of macrophage on Ti-H2O2surface is higher than that of Ti-polished. ELISA assay result revealed lower level of proinflammatory factor TNF-αand higher level of anti-inflammatory factor IL-10 on the Ti-H2O2surface compared to Ti-polished. Subsequently, immunofluorescence and western blotting analysis showed that activation of the NF-κB-TNF-αpathway might be involved in the modulation of the immune response by surface hydrophilicity. Together, these results suggested that relative high hydrophilic Ti surface might attenuate the immune response of macrophage by activating NF-κB signaling. These findings could provide new insights into designing implant devices for orthopedic applications.

scholarly journals Sodium butyrate supplementation ameliorates diabetic inflammation in db/db mice

2018 ◽  
Vol 238 (3) ◽  
pp. 231-244 ◽  
Author(s):  
You-Hua Xu ◽  
Chen-Lin Gao ◽  
Heng-Li Guo ◽  
Wen-Qian Zhang ◽  
Wei Huang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Potential Role ◽  
Barrier Integrity ◽  
Intercellular Adhesion Molecules ◽  
Junction Proteins

Endotoxemia has been recognized to be closely accompanied with type 2 diabetes mellitus (T2DM) and is responsible for many diabetic complications. Recent study suggests the potential role of butyrate, a short-chain fatty acid (SCFA) from microbiota metabolite, on T2DM. Gut-leak is a key event in diabetic-endotoxemia. To investigate if butyrate could ameliorate diabetic-endotoxemia, both in vivo and in vitro experiments were carried out in the present study. The effect of butyrate supplementation on blood HbA1c and inflammatory cytokines were determined in db/db mice; gut barrier integrity and expression of tight junction proteins were investigated both in vivo and in vitro. Oral butyrate administration significantly decreased blood HbA1c, inflammatory cytokines and LPS in db/db mice; inflammatory cell infiltration was reduced, and gut integrity and intercellular adhesion molecules were increased as detected by HE staining, immunohistochemistry and Western blot. By gut microbiota assay, ratio of Firmicutes:Bacteroidetes for gut microbiota was reduced by butyrate. In Caco-2 cells, butyrate significantly promoted cell proliferation, decreased inflammatory cytokines’ secretion, enhanced cell anti-oxidative stress ability and preserved the epithelial monocellular integrity, which was damaged by LPS. The present findings demonstrated that butyrate supplementation could ameliorate diabetic-endotoxemia in db/db mice via restoring composition of gut microbiota and preserving gut epithelial barrier integrity.

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