CCR3 Gene Knockout in Bone Marrow Cells Ameliorates Combined Allergic Rhinitis and Asthma Syndrome (CARAS) by Reducing Airway Inflammatory Cell Infiltration and Th2 Cytokines Expression in Mice Model

2021 ◽  
Author(s):  
MeiNa Dai ◽  
XinHua Zhu ◽  
Juan Yu ◽  
JiaSheng Yuan ◽  
Yv Zhu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Allergic Rhinitis ◽  
Inflammatory Cell ◽  
Bone Marrow Cells ◽  
Gene Knockout ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Th2 Cytokines ◽  
Mice Model ◽  
Marrow Cells

Abstract P295: The Inflammasome Is Involved in Myocardial Ischemia-Reperfusion Injury

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Masafumi Takahashi ◽  
Masanori Kawaguchi ◽  
Fumitake Usui ◽  
Hiroaki Kimura ◽  
Shun'ichiro Taniguchi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Myocardial Ischemia ◽  
Inflammatory Cell ◽  
Bone Marrow Cells ◽  
Cardiac Fibroblasts ◽  
Ischemia Reperfusion ◽  
Inflammatory Cell Infiltration ◽  
Inflammasome Activation ◽  
Caspase 1 ◽  
Myocardial Ischemia Reperfusion

Background: Accumulating evidence indicates that inflammation is involved in the pathophysiology of myocardial ischemia-reperfusion (I/R) injury. However, the mechanism of I/R-initiated inflammation remains to be determined. The inflammasome is a multiprotein complex consisting of nod-like receptor (NLR), apoptosis-associated speck-like adaptor protein (ASC), and caspase-1, and regulates caspase-1-dependent maturation of IL-1beta and IL-18. In the present study, we investigated the role of inflammasome in myocardial I/R injury. Methods and Results: Wild-type (WT), ASC−/−, and caspase-1−/− mice were subjected to 30 min LAD ligation, followed by reperfusion. ASC and caspase-1 were expressed at the site of myocardial I/R injury. Deficiency of ASC and caspase-1 reduced inflammatory responses, such as inflammatory cell infiltration and cytokine expression, and subsequent injuries such as infarct development, myocardial fibrosis, and dysfunction in myocardial I/R injury. To determine the contribution of inflammasome in bone marrow cells, we produced bone marrow transplant mice and found that inflammasome activation was critical not only in bone marrow cells but also in myocardial resident cells. Since myocardial damage was observed before the inflammatory cell infiltration after I/R, we hypothesized that myocardial resident cells are responsible for an initial activation of inflammasome. To test this hypothesis, we examined whether hypoxia/reoxygenation (H/R) stimuli could induce inflammasome activation in cardiac fibroblasts and cardiomyocytes in vitro. Interestingly, inflammasome activation was detected only in cardiac fibroblasts, but not in cardiomyocytes, and mediated through reactive oxygen species (ROS) and potassium efflux. Conclusion: These findings indicate that inflammasome activation in cardiac fibroblasts is essential for inflammation and injury after myocardial I/R, and suggest that the inflammasome is a potential novel therapeutic target for myocardial I/R injury.

scholarly journals MiR-574-5p alleviates sepsis-induced acute lung injury by regulating TRAF6/NF-κB pathway

2020 ◽  
Vol 19 (4) ◽  
pp. 676-682
Author(s):  
Changfu Xu ◽  
Lei Chong ◽  
Gang Yu ◽  
Hailin Zhang
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cell ◽  
Inflammatory Responses ◽  
Cecal Ligation ◽  
Cytokine Expression ◽  
Inflammatory Cell Infiltration ◽  
Luciferase Assay ◽  
Cell Infiltration ◽  
Mice Model

Purpose: To investigate the protective effect of miR-574-5p pretreatment against acute lung injury (ALI) induced by sepsis.Methods: A male C57BL/6 mouse model of sepsis-induced ALI was established by cecal ligation and puncture (CLP) and treated with miR-574-5p agomir (intravenous injection, 80 mg/kg per day, 3 days). After that, blood and lung samples were obtained for histopathological observation. Myeloperoxidase (MPO) activity, inflammatory cell infiltration, and cytokine expression were analyzed. The target gene of miR-574-5p was predicted using TargetScan prediction, and verified by luciferase assay and western blot.Results: In sepsis-induced ALI mice model, downregulation of miR-574-5p was observed. Pretreatment of miR-574-5p significantly alleviated ALI by suppressing histological damage, and reducing MPO activity and inflammatory cell infiltration, as well as decreasing cytokine expression. The  underlying mechanism was that miR-574-5p targeted TNF receptor associated factor 6 (TRAF6) and suppressed the downstream NF-κB pathway. Moreover, TRAF6 overexpression reversed the effects of miR-574-5p on ALI.Conclusion: MiR-574-5p pretreatment suppresses inflammatory responses, thus reducing lung injury induced by sepsis in mice, partly via the regulation of TRAF6 and NF-κB pathway. Therefore, this approach can potentially be used for the clinical management of ALI in humans Keywords: Sepsis, Acute lung injury, MiR-574-5p, TRAF6, NF-κB pathway

scholarly journals Muscle paralysis induces bone marrow inflammation and predisposition to formation of giant osteoclasts

2017 ◽  
Vol 313 (5) ◽  
pp. C533-C540 ◽  
Author(s):  
Brandon J. Ausk ◽  
Leah E. Worton ◽  
Kate S. Smigiel ◽  
Ronald Y. Kwon ◽  
Steven D. Bain ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Resorption ◽  
Time Course ◽  
Inflammatory Cell ◽  
Botulinum Toxin A ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Muscle Paralysis ◽  
Inflammatory Microenvironment ◽  
Tibia Bone

Transient muscle paralysis engendered by a single injection of botulinum toxin A (BTxA) rapidly induces profound focal bone resorption within the medullary cavity of adjacent bones. While initially conceived as a model of mechanical disuse, osteoclastic resorption in this model is disproportionately severe compared with the modest gait defect that is created. Preliminary studies of bone marrow following muscle paralysis suggested acute upregulation of inflammatory cytokines, including TNF-α and IL-1. We therefore hypothesized that BTxA-induced muscle paralysis would rapidly alter the inflammatory microenvironment and the osteoclastic potential of bone marrow. We tested this hypothesis by defining the time course of inflammatory cell infiltration, osteoinflammatory cytokine expression, and alteration in osteoclastogenic potential in the tibia bone marrow following transient muscle paralysis of the calf muscles. Our findings identified inflammatory cell infiltration within 24 h of muscle paralysis. By 72 h, osteoclast fusion and pro-osteoclastic inflammatory gene expression were upregulated in tibia bone marrow. These alterations coincided with bone marrow becoming permissive to the formation of osteoclasts of greater size and greater nuclei numbers. Taken together, our data are consistent with the thesis that transient calf muscle paralysis induces acute inflammation within the marrow of the adjacent tibia and that these alterations are temporally consistent with a role in mediating muscle paralysis-induced bone resorption.

scholarly journals Hepatic recruitment of macrophages promotes nonalcoholic steatohepatitis through CCR2

2012 ◽  
Vol 302 (11) ◽  
pp. G1310-G1321 ◽  
Author(s):  
Kouichi Miura ◽  
Ling Yang ◽  
Nico van Rooijen ◽  
Hirohide Ohnishi ◽  
Ekihiro Seki
Keyword(s):  
Bone Marrow ◽  
Kupffer Cells ◽  
Chemokine Receptor ◽  
Nonalcoholic Steatohepatitis ◽  
Inflammatory Cell ◽  
Therapeutic Potential ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Potent Inducer ◽  
Hepatic Macrophages

Inflammatory cell infiltration in the liver is a hallmark of nonalcoholic steatohepatitis (NASH). The chemokine-chemokine receptor interaction induces inflammatory cell recruitment. CC-chemokine receptor (CCR)2 is expressed on hepatic macrophages and hepatic stellate cells. This study aims to investigate the therapeutic potential of CCR2 to NASH. Twenty-two weeks on a choline-deficient amino acid-defined (CDAA) diet induced steatosis, inflammatory cell infiltration, and liver fibrosis with increased CCR2 and monocyte chemoattractant protein (MCP)-1 expression in the wild-type livers. The infiltrated macrophages expressed CD68, CCR2, and a marker of bone marrow-derived monocytes, Ly6C. CCR2−/− mice had less steatosis, inflammatory cell infiltration, and fibrosis, and hepatic macrophages expressing CD68 and Ly6C were decreased. Toll-like receptor (TLR)4−/−, TLR9−/−, and MyD88−/− mice had reduced hepatic macrophage infiltration with decreased MCP-1 and CCR2 expression because TLR signaling is a potent inducer of MCP-1. To assess the role of Kupffer cells at the onset of NASH, Kupffer cells were depleted by liposomal clodronate. The Kupffer cell depletion ameliorated steatohepatitis with a decrease in the MCP-1 expression and recruitment of Ly6C-expressing macrophages at the onset of NASH. Finally, to test the therapeutic potential of targeting CCR2, a CCR2 inhibitor was administered to mice on a CDAA diet. The pharmaceutical inhibition of CCR2 prevented infiltration of the Ly6C-positive macrophages, resulting in an inhibition of liver inflammation and fibrosis. We concluded that CCR2 and Kupffer cells contribute to the progression of NASH by recruiting bone marrow-derived monocytes.

scholarly journals The Influence of Bone Marrow-Secreted IL-10 in a Mouse Model of Cerulein-Induced Pancreatic Fibrosis

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Wey-Ran Lin ◽  
Siew-Na Lim ◽  
Tzung-Hai Yen ◽  
Malcolm R. Alison
Keyword(s):  
Bone Marrow ◽  
Mouse Model ◽  
Inflammatory Cell ◽  
Inflammatory Cell Infiltration ◽  
Pancreatic Fibrosis ◽  
Cell Infiltration ◽  
Collagen Deposition ◽  
Wild Type

This study aimed to understand the role of IL-10 secreted from bone marrow (BM) in a mouse model of pancreatic fibrosis. The severity of cerulein-induced inflammation, fibrosis, and the frequency of BM-derived myofibroblasts were evaluated in the pancreas of mice receiving either a wild-type (WT) BM or an IL-10 knockout (KO) BM transplantation. The area of collagen deposition increased significantly in the 3 weeks after cerulein cessation in mice with an IL-10 KO BM transplant (13.7 ± 0.6% and 18.4 ± 1.1%,p< 0.05), but no further increase was seen in WT BM recipients over this time. The percentage of BM-derived myofibroblasts also increased in the pancreas of the IL-10 KO BM recipients after cessation of cerulein (6.7 ± 1.1% and 11.9 ± 1.3%,p< 0.05), while this figure fell in WT BM recipients after cerulein withdrawal. Furthermore, macrophages were more numerous in the IL-10 KO BM recipients than the WT BM recipients after cerulein cessation (23.2 ± 2.3 versus 15.3 ± 1.7 per HPF,p< 0.05). In conclusion, the degree of fibrosis, inflammatory cell infiltration, and the number of BM-derived myofibroblasts were significantly different between IL-10 KO BM and WT BM transplanted mice, highlighting a likely role of IL-10 in pancreatitis.

596 TH1/TH2 CYTOKINES AND SOLUBLE CD30 LEVELS IN KIDNEY ALLOGRAFT PATIENTS WITH DONOR BONE MARROW CELLS INFUSION

2009 ◽  
Vol 8 (4) ◽  
pp. 269
Author(s):  
G. Pourmand ◽  
A.A. Amirzargar ◽  
G. Solgi ◽  
A. Mehrsai ◽  
M. Taherimahmoudi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Th2 Cytokines ◽  
Kidney Allograft ◽  
Donor Bone Marrow ◽  
Soluble Cd30 ◽  
Marrow Cells

scholarly journals 4-Hydroxyhalcone effects on cisplatin-induced genotoxicity model

2021 ◽  
Author(s):  
Aref Nazari ◽  
Mina Mirian ◽  
Mahmoud Aghaei ◽  
Mehdi Aliomrani
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Antineoplastic Agent ◽  
Hek293 Cells ◽  
Natural Food ◽  
Treatment Schedule ◽  
Ros Production ◽  
Mice Model ◽  
Marrow Cells

Abstract Background The genotoxicity of cisplatin (CP) as a platinum-based antineoplastic agent due to its oxidative stress induction was well known. In this research, we examined 4-hydroxychalcone (4-HCH) as a natural food that presents flavonoid effects on reactive oxygen species (ROS) production and CP-induced in vivo genotoxicity. Method and materials Cytotoxicity of CP and 4-HCH was measured on human embryonic kidney 293 cells with MTT assay. Then, intracellular ROS content at IC50 concentration of CP was measured with 2′,7′-dichlorofluorescein diacetate (DCFDA) dye. Finally, 4-HCH was administered intraperitoneally at 10 and 40 mg/kg/BW doses as a pre and post-treatment schedule in a mice model of CP genotoxicity (7 mg/kg). Acridine-orange-stained bone marrow cells were quantified for micronucleus presence examination. Results The calculated IC50 of CP and 4-HCH were reported around 19.4 and 133.6 μM, respectively, on HEK293 cells. Also, it was observed that 4-HCH at 0.2, 2 and 10 μM concentrations did not show obvious cytotoxicity. The fluorimetry confirmed that pre-treatment with 10 μM and co-treatment with 2 μM of 4-HCH could attenuate the CP-induced ROS production (P &lt; 0.05 and P &lt; 0.01, respectively). Also, the lowest micronucleated cells were seen in 10 mg/kg 4-HCH-treated group after CP exposure (39 ± 7.9, P &lt; 0.0001). Discussion Our results demonstrated the antigenotoxic action of 4-HCH in CP-treated mice bone marrow cells for the first time in both concentrations of 10 and 40 mg/kg especially in the form of co-treatment. Further studies required clinical application of this compound in a combination of CP to attenuate the normal cells’ genotoxicity side effects.

CABG and intramyocardial delivery of CD133+ bone marrow cells: 3-years follow-up on safety and efficacy

2006 ◽  
Vol 54 (S 1) ◽  
Author(s):  
C Stamm ◽  
YH Choi ◽  
A Liebold ◽  
HD Kleine ◽  
S Dunkelmann ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Safety And Efficacy ◽  
Intramyocardial Delivery ◽  
Marrow Cells
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