scholarly journals Pro-Inflammatory Stimuli Influence Expression of Intercellular Adhesion Molecule 1 in Human Anulus Fibrosus Cells through FAK/ERK/GSK3 and PKCδ Signaling Pathways

2018 ◽  
Vol 20 (1) ◽  
pp. 77 ◽  
Author(s):  
Bor-Ren Huang ◽  
Da-Tian Bau ◽  
Tzu-Sheng Chen ◽  
I-Chen Chuang ◽  
Cheng-Fang Tsai ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Immune Cells ◽  
Time Dependent ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Anulus Fibrosus ◽  
Inflammatory Stimuli ◽  
Ivd Degeneration

Objective: Intervertebral disc (IVD) degeneration and disc herniation are major causes of lower back pain, which involve the presence of inflammatory mediators and tissue invasion by immune cells. Intercellular adhesion molecule 1 (ICAM1, also termed CD54) is an adhesion molecule that mediates cell-cell interactions, particularly between immune cells and target tissue. The aim of this study was to examine the intracellular signaling pathways involved in inflammatory stimuli-induced ICAM1 expression in human anulus fibrosus (AF) cells. Methods: Quantitative reverse transcription-polymerase chain reaction (qPCR), western blotting, and flow cytometry were performed to dissect the roles of different signaling pathways in inflammatory stimuli-mediated ICAM1 expression. Results: Using qPCR and western blot analyses, a significant increase in ICAM1 expression was observed in AF cells after stimulation of lipopolysaccharide (LPS) plus interferon-gamma (IFNγ) in a time-dependent manner. Flow cytometry revealed ICAM1 upregulation on the surface of AF cells. Importantly, LPS plus IFNγ treatment also significantly promoted Chemokine ligand (CCL)2 expression, but not CCL3. The enhanced ICAM1 expression was abolished after incubation with antibody against CCL2. In AF cells, treatment with LPS plus IFNγ activated the FAK/ERK/GSK3 signaling pathways, promoted a time-dependent increase in PKCδ phosphorylation, and promoted PKCδ translocation to the nucleus. Treatment with the pharmacological PKCδ inhibitor; rottlerin, effectively blocked the enhanced productions of ICAM1 and CCL2. Conclusions: Inflammatory stimuli in AF cells are part of a specific pathophysiology in IVD degeneration and disc herniation that modulates CCL2/ICAM1 activation through the FAK/ERK/GSK3 and PKCδ signaling pathways in AF cells.

Role of macrophage SR-BI class a scavenger receptor in atherosclerosis: Crosstalk TLR4/NF-KB/ signaling pathway activation   

2019 ◽  
Vol 7 (4) ◽  
pp. 298-309
Author(s):  
Jilin Wang ◽  
Jeffrey D. Juan
Keyword(s):  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Intracellular Signaling ◽  
Scavenger Receptor ◽  
Cell Types ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Inflammatory Stimuli ◽  
Class B ◽  
Tlr4 Activation

Atherosclerosis is an inflammatory disease, and one of the culprits may be infections caused by pathogens, that may be linked to development and progression of atherosclerosis by several mechanisms. Class B scavenger receptor BI (SR-BI), an HDL receptor, SR-BI is expressed in a variety of cell types, most abundantly in steroidogenic cells and in the liver. SR-BI is also expressed in macrophages has been shown to mediate the cellular uptake of certain bacteria and may therefore play an important role in innate immunity. The innate immune response and the homeostatic network controlling cellular sterol are important implications for several common diseases, including atherosclerosis. The TLR4-independent SR-BI signaling in macrophages and the implication for its role in atherosclerosis has not yet to be investigated. Our data showed that mice lacking SR-BI are highly sensitive to form atherosclerosis than wild type mice. In addition, we showed that SR-BI-/- mice attenuated proinflammatory cytokines and chemokine response to LPS. The LPS-induced cytokine expression in both WT and SR-BI-/- was dependent on NFκB signaling pathways. One possibility is that an interaction between SR-BI and the TLR4 complex might modulate TLR4 activation and subsequent intracellular signaling pathways. The interaction of HDL and SR-BI in endothelial cells inhibits the activation of NFκB and subsequent expression of the adhesion molecules vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 to inflammatory stimuli. We conclude that SR-BI plays an important function in the atherosclerosis mechanism.

Piperine from Black Pepper Decreased the Expression of Intercellular Adhesion Molecule-1 in Macrophages

2020 ◽  
Vol 19 ◽  
Author(s):  
Nasser Gholijani ◽  
Esmaeil Hashemi ◽  
Zahra Amirghofran
Keyword(s):  
Flow Cytometry ◽  
Adhesion Molecule ◽  
Macrophage Polarization ◽  
Geometric Mean ◽  
Black Pepper ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Therapeutic Benefits ◽  
Relative Fold Change

Background: Macrophages are the main players involved in inflammation. Intercellular adhesion molecule-1 (ICAM-1) facilitates macrophage polarization prior to extravasation into inflamed tissue. Piperine a natural product derived from black pepper possess useful biological and pharmacological activities. In current study, the possible anti-inflammatory effect of piperine on the expression of ICAM-1 on J774.1 murine macrophage cell line was investigated. Methods: Lipopolysaccharide (LPS)-stimulated J774.1 cells were cultured in the presence of different concentrations of piperine to examine the changes in ICAM-1 expression by real-time PCR and flow cytometry. Results: We found that piperine decreased ICAM-1 gene expression level from 2.4 ± 0.25 RFC (relative fold change) in LPS-only treated cells to 0.85 ± 0.525 RFC at 1μg/ml (p<0.05), 0.43 ± 0.27 RFC at 10μg/ml (p<0.01), and 0.26 ± 0.25 RFC at 20μg/ml (p<0.01). In flow cytometry, piperine at all concentrations significantly decreased ICAM-1 surface expressions (P<0.05). The geometric mean fluorescence intensity (g-MFI) in LPS-only treated cells (792 ± 57.3) decreased to 482±70 gMFI at 20 µg/ml piperine. Conclusion: According to the results of this study, by decreasing the expression of ICAM-1, piperine is suggested as a candidate to reduce inflammation and has the potential for therapeutic benefits for immune-mediated diseases.

scholarly journals Invasion of Human Mucosal Epithelial Cells by Neisseria gonorrhoeae Upregulates Expression of Intercellular Adhesion Molecule 1 (ICAM-1)

1999 ◽  
Vol 67 (3) ◽  
pp. 1149-1156 ◽  
Author(s):  
Gary A. Jarvis ◽  
Jing Li ◽  
Karen V. Swanson
Keyword(s):  
Flow Cytometry ◽  
B Cells ◽  
Epithelial Cells ◽  
Neisseria Gonorrhoeae ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
Invasive Strain

ABSTRACT Infection of the mucosa by Neisseria gonorrhoeaeinvolves adherence to and invasion of epithelial cells. Little is known, however, about the expression by mucosal epithelial cells of molecules that mediate cellular interactions between epithelial cells and neutrophils at the site of gonococcal infection. The aim of this study was to determine the expression of intercellular adhesion molecule 1 (ICAM-1) by epithelial cells during the process of gonococcal invasion. The highly invasive strain FA1090 and the poorly invasive strain MS11 were incubated with human endometrial adenocarcinoma (HEC-1-B) or human cervical carcinoma (ME-180) epithelial cells, after which ICAM-1 expression was measured by flow cytometry. After 15 h of infection with FA1090, expression of ICAM-1 increased 4.7- and 2.1-fold for HEC-1-B and ME-180 cells, respectively, whereas 15 h of infection of HEC-1-B cells with MS11 increased ICAM-1 expression only 1.6-fold. ICAM-1 expression was restricted to the cell surface, since no soluble ICAM-1 was detected. The distribution of staining was heterogeneous and mimicked that seen after treatment of HEC-1-B cells with the ICAM-1 agonist tumor necrosis factor alpha (TNF-α) in the absence of bacteria. PCR and dot blot analyses of ICAM-1 mRNA showed no change in levels over time in response to infection. Although TNF-α was produced by HEC-1-B cells after infection, the extent of ICAM-1 upregulation was not affected by neutralizing anti-TNF-α antiserum. Dual-fluorescence flow cytometry showed that the cells with the highest levels of ICAM-1 expression were cells with associated gonococci. We conclude that epithelial cells upregulate the expression of ICAM-1 in response to infection with invasive gonococci. On the mucosa, upregulation of ICAM-1 by infected epithelial cells may function to maintain neutrophils at the site of infection, thereby reducing further invasion of the mucosa by gonococci.

Role of intercellular adhesion molecule-1 in antigen-induced lung inflammation in brown Norway rats

1996 ◽  
Vol 271 (2) ◽  
pp. L267-L276
Author(s):  
I. M. Richards ◽  
K. P. Kolbasa ◽  
G. E. Winterrowd ◽  
C. A. Hatfield ◽  
S. L. Vonderfecht ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Adhesion Molecule ◽  
Lung Inflammation ◽  
Ex Vivo ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Brown Norway ◽  
Intercellular Adhesion Molecule 1

We investigated the involvement of intercellular adhesion molecule-1 (ICAM-1; CD54) in ovalbumin (OA) antigen-induced lung inflammation in sensitized Brown Norway (BN) rats by using flow cytometry and in vivo treatment with a murine monoclonal antibody (MAb), 1A29, directed against rat ICAM-1. OA-challenge induced an eosinophil and lymphocyte-rich accumulation of leukocytes into the airway lumen. Between 75 and 90% of the T cells in bronchoalveolar lavage (BAL) fluid after challenge expressed CD54 and CD11a and were of the memory phenotype. 1A29 treatment produced dose-related increases in circulating 1A29 and blood neutrophils. In the BAL fluid of 1A29-treated animals, significant (P < 0.05) reductions in the numbers of eosinophils and lymphocytes, but not neutrophils or alveolar macrophages, were observed in association with a reduced inflammatory pathology in lung tissue. 1A29 administration reduced the number of detectable ICAM-1 binding sites on T cells in peripheral blood and BAL fluid examined ex vivo by flow cytometry. We conclude that ICAM-1 is critically important for the antigen-specific recruitment of eosinophils and lymphocytes into the lungs.

Sign in / Sign up

Export Citation Format

Share Document