scholarly journals Immunoenhancement of Edible Fungal Polysaccharides (Lentinan, Tremellan, and Pachymaran) on Cyclophosphamide-Induced Immunosuppression in Mouse Model

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Qian Zhang ◽  
Renhuai Cong ◽  
Minghua Hu ◽  
Yanhong Zhu ◽  
Xiangliang Yang
Keyword(s):  
Flow Cytometry ◽  
Mouse Model ◽  
Protective Effect ◽  
Biological Activities ◽  
Serum Antibody ◽  
Peritoneal Macrophages ◽  
Immunomodulatory Effect ◽  
Immune Activity ◽  
Anti Inflammatory ◽  
Fungal Polysaccharides

Fungal polysaccharides display a variety of important biological activities, including anti-inflammatory, antitumor, and immune-stimulating activities. The aim of present study was to investigate the immunomodulatory effect of fungal polysaccharides on cyclophosphamide-induced immunosuppression in mice. Mice were pretreated orally with lentinan, tremellan, pachymaran, or a mixture of the three, respectively. The results showed that pretreatments with polysaccharides significantly increased the thymus index in cyclophosphamide-induced immunosuppression mice. The level of the cytokine IL-10 in sera of cyclophosphamide-induced mice was decreased after pretreatments of polysaccharides. Flow cytometry results showed that pretreatments with polysaccharides enhanced the phagocytosis of peritoneal macrophages in mice. The increased levels of serum antibody IgG and IgM were observed in the groups pretreated with polysaccharides. Our work demonstrated that the treatment of polysaccharides elicited strong immune activity and a protective effect against cyclophosphamide-induced immunosuppression.

scholarly journals Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation

2017 ◽  
Vol 313 (4) ◽  
pp. L710-L721 ◽  
Author(s):  
Yunbo Ke ◽  
Olga V. Oskolkova ◽  
Nicolene Sarich ◽  
Yufeng Tian ◽  
Albert Sitikov ◽  
...  
Keyword(s):  
Protective Effect ◽  
Vascular Endothelial Cells ◽  
Biological Activities ◽  
Cell Monolayer ◽  
Endothelial Permeability ◽  
In Vivo Model ◽  
Barrier Dysfunction ◽  
Anti Inflammatory

Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory effects of PGE2 and PGI2 on vascular endothelial cells (EC). Yet, the effects of other PG members on EC barrier and inflammatory activation have not been systematically analyzed. This study compared effects of PGE2, PGI2, PGF2α, PGA2, PGJ2, and PGD2 on human pulmonary EC. EC permeability was assessed by measurements of transendothelial electrical resistance and cell monolayer permeability for FITC-labeled tracer. Anti-inflammatory effects of PGs were evaluated by analysis of expression of adhesion molecule ICAM1 and secretion of soluble ICAM1 and cytokines by EC. PGE2, PGI2, and PGA2 exhibited the most potent barrier-enhancing effects and most efficient attenuation of thrombin-induced EC permeability and contractile response, whereas PGI2 effectively suppressed thrombin-induced permeability but was less efficient in the attenuation of prolonged EC hyperpermeability caused by interleukin-6 or bacterial wall lipopolysaccharide, LPS. PGD2 showed a modest protective effect on the EC inflammatory response, whereas PGF2α and PGJ2 were without effect on agonist-induced EC barrier dysfunction. In vivo, PGE2, PGI2, and PGA2 attenuated LPS-induced lung inflammation, whereas PGF2α and PGJ2 were without effect. Interestingly, PGD2 exhibited a protective effect in the in vivo model of LPS-induced lung injury. This study provides a comprehensive analysis of barrier-protective and anti-inflammatory effects of different prostaglandins on lung EC in vitro and in vivo and identifies PGE2, PGI2, and PGA2 as prostaglandins with the most potent protective properties.

scholarly journals Marinobufagenin Inhibits Neutrophil Migration and Proinflammatory Cytokines

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Deyse C. M. Carvalho ◽  
Luiz Henrique Agra Cavalcante-Silva ◽  
Éssia de A. Lima ◽  
José G. F. M. Galvão ◽  
Anne K. de A. Alves ◽  
...  
Keyword(s):  
Cell Migration ◽  
Proinflammatory Cytokines ◽  
Proinflammatory Cytokine ◽  
Biological Activities ◽  
Neutrophil Migration ◽  
Peritoneal Macrophages ◽  
Cytokine Levels ◽  
Anti Inflammatory

Cardiotonic steroids, such as ouabain and digoxin, are known to bind to Na+/K+-ATPase and to promote several biological activities, including anti-inflammatory activity. However, there are still no reports in the literature about inflammation and marinobufagenin, a cardiotonic steroid from the bufadienolide family endogenously found in mammals. Therefore, the aim of this work was to analyze, in vivo and in vitro, the role of marinobufagenin in acute inflammation. Swiss mice were treated with 0.56 mg/kg of marinobufagenin intraperitoneally (i.p.) and zymosan (2 mg/mL, i.p.) was used to induce peritoneal inflammation. Peritoneal fluid was collected and used for counting cells by optical microscopy and proinflammatory cytokine quantification (IL-1β, IL-6, and TNF-α) by immunoenzymatic assay (ELISA). Zymosan stimulation, as expected, induced increased cell migration and proinflammatory cytokine levels in the peritoneum. Marinobufagenin treatment reduced polymorphonuclear cell migration and IL-1β and IL-6 levels in the peritoneal cavity, without interfering in TNF-α levels. In addition, the effect of marinobufagenin was evaluated using peritoneal macrophages stimulated by zymosan (0.2 mg/mL) in vitro. Marinobufagenin treatment at different concentrations (10, 100, 1000, and 10000 nM) showed no cytotoxic effect on peritoneal macrophages. Interestingly, the lowest concentration, which did not inhibit Na+/K+-ATPase activity, attenuated proinflammatory cytokines IL-1β, IL-6, and TNF-α levels. To investigate the putative mechanism of action of marinobufagenin, the expression of surface molecules (TLR2 and CD69) and P-p38 MAPK were also evaluated, but no significant effect was observed. Thus, our results suggest that marinobufagenin has an anti-inflammatory role in vivo and in vitro and reveals a novel possible endogenous function of this steroid in mammals.

Regulatory Role of Host IL-17 Via Control of Host Macrophage Activation Contributes to Less Acute Gvhd

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4669-4669
Author(s):  
Rie Kuroda ◽  
Katsuaki Sato ◽  
Hideaki Maeba ◽  
Toshihiro Fujiki ◽  
Shintaro Mase ◽  
...  
Keyword(s):  
Protective Effect ◽  
Inflammatory Cytokine ◽  
Acute Gvhd ◽  
Conflicts Of Interest ◽  
Chronic Gvhd ◽  
Paneth Cell ◽  
Peritoneal Macrophages ◽  
Regulatory Role ◽  
Hematopoietic Stem ◽  
Anti Inflammatory

Abstract Abstract 4669 IL-17 has emerged as a key pro-inflammatory cytokine, however, recent studies demonstrated that IL-17 has also anti-inflammatory effects. In addition, a wide variety of IL-17 producing cells are identified not only in T-cells but also in subpopulation of monocytes and macrophages, mast cells, Paneth cell in the gut so on. Therefore, IL-17 mediated immune responses are becoming much more complicated. In hematopoietic stem cell transplantation, we have reported that host-derived IL-17 has a protective effect against acute graft-versus-host disease (GVHD) using rodent models, in contrast, donor-BM-derived IL-17 exacerbates chronic GVHD. In acute GVHD model, lethally irradiated IL-17 knockout (KO) recipient mice receiving allogeneic BM with low dose splenocytes developed more severe acute gut GVHD compared to wild type (WT) host mice and finally half of them died (p<0.05). Much higher number of infiltrated monocyte/macrophage cluster was observed in spleen and gut in IL-17 KO host mice. Furthermore, residual host-typed peritoneal macrophages in IL-17 KO host mice were highly activated with the expression of TNF-α, while activation of donor-typed macrophages was much less with the production of anti-inflammatory cytokine IL-10. It suggested that these activated and increased macrophages might deeply involve in the pathogenesis of lethal GVHD. To test this, IL-17 KO recipient mice were given lipoCL2MDP intraperitoneally on day -7 before BMT to deplete host macrophages. As shown in the figure below, the macrophages depleted IL-17 KO host mice given splenocytes to induce lethal GVHD showed a significant survival benefit compared with IL-17 KO mice without depletion of macrophages. In conclusion, host IL-17 has a protective effect against acute GVHD with suppression of the activated macrophages. This is the first report that IL-17 has the immuno-regulatory role via control of activated host macrophages in acute GVHD. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Piperine Plays an Anti-Inflammatory Role inStaphylococcus aureusEndometritis by Inhibiting Activation of NF-κB and MAPK Pathways in Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Wen-jun Zhai ◽  
Zhen-biao Zhang ◽  
Nian-nian Xu ◽  
Ying-fang Guo ◽  
Changwei Qiu ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Biological Activities ◽  
Dependent Manner ◽  
Pathogenic Microorganisms ◽  
Histopathological Changes ◽  
Natural Medicine ◽  
Anti Inflammatory ◽  
Dose Dependent

Endometritis is commonly caused by pathogenic microorganisms, includingStaphylococcus aureus(S. aureus). Piperine, which is a natural medicine, has shown a variety of biological activities. To explore the effect and mechanism of piperine onS. aureusendometritis, a mouse model ofS. aureusendometritis was successfully established in the present study. Histopathological changes were observed with H&E staining, cytokines were analyzed by ELISA, mRNA was analyzed by qPCR, and proteins were detected by western blot. The results showed that piperine could significantly alleviate inflammatory injury inS. aureusendometritis. The qPCR and ELISA results showed that piperine effectively reduced theS. aureus-induced overexpression of TNF-α, IL-1β, and IL-6 but increased the expression of IL-10. TheS. aureus-induced inflammation was related to TLR-2 and TLR-4 because the results showed that their expression was increased inS. aureusinfection but then decreased with piperine treatment. To further confirm that piperine caused an anti-inflammatory response by targeting NF-κB and MAPKs, the expression of I-κB, p65, p38, ERK, and JNK was measured. The phosphorylation of I-κB, p65, p38, ERK, and JNK was inhibited by piperine in a dose-dependent manner. All of the results indicated that piperine may be a potential anti-inflammatory drug both in endometritis and in otherS. aureus-induced diseases.

scholarly journals IFN-τDisplays Anti-Inflammatory Effects onStaphylococcus aureusEndometritis via Inhibiting the Activation of the NF-κB and MAPK Pathways in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Zhenbiao Zhang ◽  
Yingfang Guo ◽  
Yuzhu Liu ◽  
Chengye Li ◽  
Mengyao Guo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protective Effect ◽  
Inflammatory Cytokine ◽  
Inflammatory Diseases ◽  
Potential Drug ◽  
Histopathological Changes ◽  
Uterine Infection ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Inflammatory Effect

The aim of the present study was to determine the anti-inflammatory effect of IFN-τon endometritis using a mouse model ofS. aureus-induced endometritis and to elucidate the mechanism of action underlying these effects. In the present study, the effect of IFN-τonS. aureusgrowth was monitored by turbidimeter at 600 nm. IFN-τdid not affectS. aureusgrowth. The histopathological changes indicated that IFN-τhad a protective effect on uterus tissues withS. aureusinfection. The ELISA and qPCR results showed the production of the proinflammatory cytokines TNF-α, IL-1β, and IL-6 was decreased with IFN-τtreatment. In contrast, the level of the anti-inflammatory cytokine IL-10 was increased. We further studied the signaling pathway associated with these observations, and the qPCR results showed that the expression of TLR2 was repressed by IFN-τ. Furthermore, the western blotting results showed the phosphorylation of IκB, NF-κB p65, and MAPKs (p38, JNK, and ERK) was inhibited by IFN-τtreatment. The results suggested that IFN-τmay be a potential drug for the treatment of uterine infection due toS. aureusor other infectious inflammatory diseases.

scholarly journals Nuezhenide Exerts Anti-Inflammatory Activity through the NF-κB Pathway

2020 ◽  
Vol 14 (1) ◽  
pp. 101-111
Author(s):  
Qin-Qin Wang ◽  
Shan Han ◽  
Xin-Xing Li ◽  
Renyikun Yuan ◽  
Youqiong Zhuo ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Biological Activities ◽  
Immunofluorescence Assay ◽  
Inflammatory Activity ◽  
Raw264.7 Cells ◽  
Phosphorylated Proteins ◽  
Tnf Α ◽  
Antioxidative Effects ◽  
Anti Inflammatory ◽  
Ilex Pubescens

Background: Nuezhenide (NZD), an iridoid glycoside isolated from Ilex pubescens Hook. & Arn. var. kwangsiensis Hand.-Mazz. used as a traditional Chinese medicine of clearing away heat and toxic materials, displays a variety of biological activities like anti-tumor, antioxidant, and protecting live. However, few studies involving anti-inflammatory activity and mechanism of NZD are reported. In the present study, NZD’s anti-inflammatory and antioxidative effects were illustrated. Objective: This study aims to test the hypothesis that NZD suppresses LPS-induced inflammation by targeting the NF-κB pathway in RAW264.7 cells. Methods: LPS-stimulated RAW264.7 cells were employed to detect the effect of NZD on cytokine releases by ELISA. Protein expression levels of related molecular markers were quantitated by western blotting analysis. The levels of ROS, NO, and Ca2+ were detected by the flow cytometry. The changes in mitochondrial reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were observed and verified by a fluorescence microscopy. Using immunofluorescence assay, the translocation of NF-κB/p65 from the cytoplasm into the nucleus was determined by a confocal microscopy. Results: NZD exhibited anti-inflammatory activity and reduced the release of inflammatory cytokines such as nitrite, TNF-α, and IL6. NZD suppressed the expression of the phosphorylated proteins like IKKα/β, IκBα, and p65. In addition, the flow cytometry results indicated that NZD inhibited the levels of ROS, NO, and Ca2+ in LPS-stimulated RAW264.7 cells. JC-1 assay data showed that NZD reversed LPS-induced MMP loss. Furthermore, NZD suppressed LPS-induced NF-B/p65 translocation from the cytoplasm into the nucleus. Conclusions: NZD exhibits anti-inflammatory effects via the NF-κB pathway in RAW264.7 cells.

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