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

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.

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

Infection and Immunity ◽

10.1128/iai.67.3.1149-1156.1999 ◽

1999 ◽

Vol 67 (3) ◽

pp. 1149-1156 ◽

Cited By ~ 21

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.

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

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1996.271.2.l267 ◽

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.

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