Critical Role of TNF-α-Induced Macrophage VEGF and iNOS Production in the Experimental Corneal Neovascularization

2012 ◽  
Vol 53 (7) ◽  
pp. 3516 ◽  
Author(s):  
Peirong Lu ◽  
Longbiao Li ◽  
Gaoqin Liu ◽  
Tomohisa Baba ◽  
Yuko Ishida ◽  
...  
Keyword(s):  
Critical Role ◽  
Corneal Neovascularization ◽  
Tnf Α ◽  
Inos Production

IL-36R ligands are potent regulators of dendritic and T cells

Blood ◽  
2011 ◽  
Vol 118 (22) ◽  
pp. 5813-5823 ◽  
Author(s):  
Solenne Vigne ◽  
Gaby Palmer ◽  
Céline Lamacchia ◽  
Praxedis Martin ◽  
Dominique Talabot-Ayer ◽  
...  
Keyword(s):  
T Cells ◽  
Mhc Class Ii ◽  
Critical Role ◽  
T Helper ◽  
Innate And Adaptive Immunity ◽  
Murine Bone Marrow ◽  
Intracellular Signals ◽  
Tnf Α ◽  
Ifn Γ

Abstract IL-36α (IL-1F6), IL-36β (IL-1F8), and IL-36γ (IL-1F9) are members of the IL-1 family of cytokines. These cytokines bind to IL-36R (IL-1Rrp2) and IL-1RAcP, activating similar intracellular signals as IL-1, whereas IL-36Ra (IL-1F5) acts as an IL-36R antagonist (IL-36Ra). In this study, we show that both murine bone marrow-derived dendritic cells (BMDCs) and CD4+ T lymphocytes constitutively express IL-36R and respond to IL-36α, IL-36β, and IL-36γ. IL-36 induced the production of proinflammatory cytokines, including IL-12, IL-1β, IL-6, TNF-α, and IL-23 by BMDCs with a more potent stimulatory effect than that of other IL-1 cytokines. In addition, IL-36β enhanced the expression of CD80, CD86, and MHC class II by BMDCs. IL-36 also induced the production of IFN-γ, IL-4, and IL-17 by CD4+ T cells and cultured splenocytes. These stimulatory effects were antagonized by IL-36Ra when used in 100- to 1000-fold molar excess. The immunization of mice with IL-36β significantly and specifically promoted Th1 responses. Our data thus indicate a critical role of IL-36R ligands in the interface between innate and adaptive immunity, leading to the stimulation of T helper responses.

Epicatechin attenuates doxorubicin-induced brain toxicity: Critical role of TNF-α, iNOS and NF-κB

2011 ◽  
Vol 86 (1-2) ◽  
pp. 22-28 ◽  
Author(s):  
Rasha H. Mohamed ◽  
Rehab A. Karam ◽  
Mona G. Amer
Keyword(s):  
Critical Role ◽  
Tnf Α

scholarly journals Effect Of Hesperidin In Bleomycin-Induced Pulmonary Fibrosis In Rats: Critical Role Of NRF-2, TNF-Α, AND IL-1Β

2017 ◽  
Vol 20 (9) ◽  
pp. A887-A888 ◽  
Author(s):  
AD Kandhare ◽  
A Mukherjee ◽  
SL Bodhankar
Keyword(s):  
Pulmonary Fibrosis ◽  
Critical Role ◽  
Tnf Α

scholarly journals Critical role of host γδ T cells in experimental acute graft-versus-host disease

Blood ◽  
2005 ◽  
Vol 106 (2) ◽  
pp. 749-755 ◽  
Author(s):  
Yoshinobu Maeda ◽  
Pavan Reddy ◽  
Kathleen P. Lowler ◽  
Chen Liu ◽  
Dennis Keith Bishop ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Graft Versus Host Disease ◽  
Critical Role ◽  
Γδ T Cells ◽  
Allogeneic Bone ◽  
Host Disease ◽  
Graft Versus Host ◽  
Tnf Α

Abstract γδ T cells localize to target tissues of graft-versus-host disease (GVHD) and therefore we investigated the role of host γδ T cells in the pathogenesis of acute GVHD in several well-characterized allogeneic bone marrow transplantation (BMT) models. Depletion of host γδ T cells in wild-type (wt) B6 recipients by administration of anti-T-cell receptor (TCR) γδ monoclonal antibody reduced GVHD, and γδ T-cell-deficient (γδ-/-) BM transplant recipients experienced markedly improved survival compared with normal controls (63% vs 10%, P < .001). γδ T cells were responsible for this difference because reconstitution of γδ-/- recipients with γδ T cells restored GVHD mortality. γδ-/- recipients showed decreased serum levels of tumor necrosis factor α (TNF-α), less GVHD histopathologic damage, and reduced donor T-cell expansion. Mechanistic analysis of this phenomenon demonstrated that dendritic cells (DCs) from γδ-/- recipients exhibited less allostimulatory capacity compared to wt DCs after irradiation. Normal DCs derived from BM caused greater allogeneic T-cell proliferation when cocultured with γδ T cells than DCs cocultured with medium alone. This enhancement did not depend on interferon γ (IFN-γ), TNF-α, or CD40 ligand but did depend on cell-to-cell contact. These data demonstrated that the host γδ T cells exacerbate GVHD by enhancing the allostimulatory capacity of host antigen-presenting cells. (Blood. 2005;106:749-755)

Effects of diesel exhaust particles on macrophage polarization

2016 ◽  
Vol 36 (4) ◽  
pp. 412-420 ◽  
Author(s):  
N Labranche ◽  
C El Khattabi ◽  
G Berkenboom ◽  
S Pochet
Keyword(s):  
Mrna Expression ◽  
Diesel Exhaust ◽  
Macrophage Polarization ◽  
Critical Role ◽  
Diesel Exhaust Particles ◽  
Western Blots ◽  
Cardiovascular Morbidity And Mortality ◽  
Tnf Α ◽  
Exhaust Particles

Background: Exposure to diesel exhaust particles (DEP) has long been associated with increased cardiovascular morbidity and mortality. The development of DEP toxicity seems to be linked to inflammation in which macrophages play a critical role. Macrophages can be polarized into proinflammatory M1 or anti-inflammatory M2 macrophages. The aim of this study was to identify the role of inflammation in DEP-induced toxicity by assessing the effects of DEP on macrophage polarization. Methods: Monocyte-derived macrophages (Mϕ) were stimulated with interferon γ and lipopolysaccharide or interleukin (IL)-4 to obtain M1 and M2 subtypes, respectively. To test the polarization capacity of DEP, Mϕ cells were exposed to DEP and compared to Mϕ, M1, and M2. We also studied the effects of DEP on already-polarized M1 or M2. The M1 markers assessed were tumor necrosis factor α (TNF-α) and IL-1β, while the M2 markers were the mannose receptor C type 1 (MRC-1) and transglutaminase 2 (TGM2). Results: Western blots revealed a 31 kDa band corresponding to pro-IL-1β, but only in M1-polarized macrophages. In M1, we also observed an upregulation of TNF-α messenger RNA (mRNA) expression. MRC-1 and TGM2 mRNA expression were only significantly enhanced in M2. DEP had no effect on any of the M1/M2 markers assessed. Moreover, DEP were not able to modify the phenotype of already-polarized M1 or M2. Conclusion: Mϕ incubation with DEP did not have any effect on macrophage polarization, at least on the markers assessed in this study, namely, TNF-α/IL-1β for M1, and MRC-1/TGM2 for M2. Hence, these data argue against an important role of inflammation in DEP-induced vascular toxicity.

scholarly journals Limited Role of Mincle in the Host Defense against Infection with Cryptococcus deneoformans

2020 ◽  
Vol 88 (11) ◽  
Author(s):  
Yuki Sato ◽  
Ko Sato ◽  
Hideki Yamamoto ◽  
Jun Kasamatsu ◽  
Tomomitsu Miyasaka ◽  
...  
Keyword(s):  
Host Defense ◽  
Early Stage ◽  
Critical Role ◽  
Yeast Cells ◽  
Dependent Manner ◽  
Th2 Response ◽  
Lectin Receptors ◽  
Cryptococcal Infection ◽  
Tnf Α

ABSTRACT Cryptococcus deneoformans is an opportunistic fungal pathogen that frequently causes fatal meningoencephalitis in patients with impaired cell-mediated immune responses such as AIDS. Caspase-associated recruitment domain 9 (CARD9) plays a critical role in the host defense against cryptococcal infection, suggesting the involvement of one or more C-type lectin receptors (CLRs). In the present study, we analyzed the role of macrophage-inducible C-type lectin (Mincle), one of the CLRs, in the host defense against C. deneoformans infection. Mincle expression in the lungs of wild-type (WT) mice was increased in the early stage of cryptococcal infection in a CARD9-dependent manner. In Mincle gene-disrupted (Mincle KO) mice, the clearance of this fungus, pathological findings, Th1/Th2 response, and antimicrobial peptide production in the infected lungs were nearly comparable to those in WT mice. However, the production of interleukin-22 (IL-22), tumor necrosis factor alpha (TNF-α), and IL-6 and the expression of AhR were significantly decreased in the lungs of Mincle KO mice compared to those of WT mice. In in vitro experiments, TNF-α production by bone marrow-derived dendritic cells was significantly decreased in Mincle KO mice. In addition, the disrupted lysates of C. deneoformans, but not those of whole yeast cells, activated Mincle-triggered signaling in an assay with a nuclear factor of activated T cells (NFAT)-green fluorescent protein (GFP) reporter cells expressing this receptor. These results suggest that Mincle may be involved in the production of Th22-related cytokines at the early stage of cryptococcal infection, although its role may be limited in the host defense against infection with C. deneoformans.

scholarly journals Critical role of TNF-α in cerebral aneurysm formation and progression to rupture

2014 ◽  
Vol 11 (1) ◽  
pp. 77 ◽  
Author(s):  
Robert M Starke ◽  
Nohra Chalouhi ◽  
Pascal M Jabbour ◽  
Stavropoula I Tjoumakaris ◽  
L Gonzalez ◽  
...  
Keyword(s):  
Cerebral Aneurysm ◽  
Critical Role ◽  
Aneurysm Formation ◽  
Tnf Α

MSCs inhibits the angiogenesis of HUVECs through the miR-211/Prox1 pathway

2019 ◽  
Vol 166 (1) ◽  
pp. 107-113 ◽  
Author(s):  
Jian Pan ◽  
Xianglong Wang ◽  
Dequan Li ◽  
Jianmin Li ◽  
Zipei Jiang
Keyword(s):  
Umbilical Vein ◽  
Critical Role ◽  
Corneal Opacity ◽  
Corneal Neovascularization ◽  
Inhibitory Effect ◽  
Tube Formation ◽  
Prox1 Expression ◽  
Umbilical Vein Endothelial Cells

Abstract The aim of this study was to investigate the effect of mesenchymal stem cells (MSCs) on the angiogenesis of human umbilical vein endothelial cells (HUVECs). MSCs were subconjunctival injected into rat corneal alkali burn models. Their impacts on the degree of corneal neovascularization (CNV) and corneal opacity were evaluated at 3, 6, 9 and 12 days after injection. An in vitro experiment of MSCs affecting HUVECs angiogenesis was performed and evaluated using the tube formation assay. The results showed that both CNV and corneal opacity were decreased in rats after MSCs injection. In HUVECs, angiogenesis of cells was inhibited by miR-211 overexpression. miR-211 negatively regulated Prox1 expression. Knockdown of miR-211 blocked the decrease of Prox1 expression induced by MSCs and the inhibitory effect of MSCs on the angiogenesis of HUVECs. The critical role of miR-211 in MSCs inhibition of corneal angiogenesis was confirmed in rat experiments. We concluded that MSCs inhibited the angiogenesis of HUVEC through miR-211 mediating the down-regulation of Prox1.

Critical Role of IP-10 on Reducing Experimental Corneal Neovascularization

2014 ◽  
Vol 40 (9) ◽  
pp. 891-901 ◽  
Author(s):  
Gaoqin Liu ◽  
Wenpeng Zhang ◽  
Yanhui Xiao ◽  
Peirong Lu
Keyword(s):  
Critical Role ◽  
Corneal Neovascularization
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