scholarly journals Sulfur‑containing amino acids in aged garlic extract inhibit inflammation in human gingival epithelial cells by suppressing intercellular adhesion molecule‑1 expression and IL‑6 secretion

2019 ◽  
Author(s):  
Masahiro Ohtani ◽  
Tsubasa Nishimura
Keyword(s):  
Amino Acids ◽  
Epithelial Cells ◽  
Adhesion Molecule ◽  
Intercellular Adhesion Molecule ◽  
Aged Garlic Extract ◽  
Intercellular Adhesion Molecule 1 ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells ◽  
Sulfur Containing ◽  
Aged Garlic

scholarly journals Intercellular Adhesion Molecule 1-Dependent Activation of Interleukin 8 Expression in Candida albicans-Infected Human Gingival Epithelial Cells

2005 ◽  
Vol 73 (1) ◽  
pp. 622-626 ◽  
Author(s):  
Hiroshi Egusa ◽  
Hiroki Nikawa ◽  
Seicho Makihira ◽  
Anahid Jewett ◽  
Hirofumi Yatani ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Epithelial Cells ◽  
Adhesion Molecule ◽  
Defense Mechanism ◽  
Intercellular Adhesion ◽  
Interleukin 8 ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Gingival Epithelial Cells ◽  
Human Gingival Epithelial Cells

ABSTRACT Increased induction of interleukin 8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by oral epithelial cells may play a role in the host defense mechanism in oropharyngeal candidiasis; however, little is known about the expression feature of these molecules on human gingival epithelial cells (HGECs) during Candida albicans infection. In this report we present evidence that neutralization with antibody against ICAM-1 inhibited both the adherence of C. albicans to HGECs and the Candida-induced production of IL-8, suggesting a role for ICAM-1 in recognition and signaling in HGECs to express IL-8 upon infection with C. albicans.

Possible requirement of intercellular adhesion molecule-1 for invasion of gingival epithelial cells byTreponema medium

2007 ◽  
Vol 53 (11) ◽  
pp. 1232-1238 ◽  
Author(s):  
Riyoko Tamai ◽  
Yasuyuki Asai ◽  
Atsushi Kawabata ◽  
Toshitaka Akisaka ◽  
Tomohiko Ogawa
Keyword(s):  
Epithelial Cells ◽  
Adhesion Molecule ◽  
Periodontal Diseases ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Principal Role ◽  
Gingival Epithelial Cells ◽  
Toll Like Receptor 2 ◽  
Human Gingival Epithelial Cells

Oral treponemes are members of the spirochete family of bacteria associated with periodontal diseases. In the present study, we demonstrate that intercellular adhesion molecule-1 (ICAM-1) on human gingival epithelial cells (HGEC) contributed to the invasion of Treponema medium , a medium-sized oral Treponema, into those cells. The quantity of T. medium in HGEC was found to peak at 2 h after inoculation and then decreased gradually. Immunofluorescence microscopy findings showed that the bacteria were colocalized with ICAM-1 on HGEC. Furthermore, knockdown of ICAM-1 in HGEC resulted in inhibition of T. medium invasion by RNA interference, whereas that of Toll-like receptor 2 did not. These results suggest that ICAM-1 may be required for the invasion of T. medium into HGEC, and they indicate that the molecule plays a principal role in the primary stages of the development and progression of chronic periodontitis.

scholarly journals Interleukin-8 and Intercellular Adhesion Molecule 1 Regulation in Oral Epithelial Cells by Selected Periodontal Bacteria: Multiple Effects of Porphyromonas gingivalis via Antagonistic Mechanisms

2001 ◽  
Vol 69 (3) ◽  
pp. 1364-1372 ◽  
Author(s):  
George T.-J. Huang ◽  
Daniel Kim ◽  
Jonathan K.-H. Lee ◽  
Howard K. Kuramitsu ◽  
Susan Kinder Haake
Keyword(s):  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Interleukin 8 ◽  
Intercellular Adhesion Molecule ◽  
Mrna Levels ◽  
Periodontal Pathogens ◽  
Intercellular Adhesion Molecule 1 ◽  
Gingival Epithelial Cells

ABSTRACT Interaction of bacteria with mucosal surfaces can modulate the production of proinflammatory cytokines and adhesion molecules produced by epithelial cells. Previously, we showed that expression of interleukin-8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by gingival epithelial cells increases following interaction with several putative periodontal pathogens. In contrast, expression of IL-8 and ICAM-1 is reduced after Porphyromonas gingivalis ATCC 33277 challenge. In the present study, we investigated the mechanisms that govern the regulation of these two molecules in bacterially infected gingival epithelial cells. Experimental approaches included bacterial stimulation of gingival epithelial cells by either a brief challenge (1.5 to 2 h) or a continuous coculture throughout the incubation period. The kinetics of IL-8 and ICAM-1 expression following brief challenge were such that (i) secretion of IL-8 by gingival epithelial cells reached its peak 2 h following Fusobacterium nucleatum infection whereas it rapidly decreased within 2 h after P. gingivalis infection and remained decreased up to 30 h and (ii) IL-8 and ICAM-1 mRNA levels were up-regulated rapidly 2 to 4 h postinfection and then decreased to basal levels 8 to 20 h after infection with either Actinobacillus actinomycetemcomitans, F. nucleatum, or P. gingivalis. Attenuation of IL-8 secretion was facilitated by adherent P. gingivalis strains. The IL-8 secreted from epithelial cells after F. nucleatum stimulation could be down-regulated by subsequent infection with P. gingivalisor its culture supernatant. Although these results suggested that IL-8 attenuation at the protein level might be associated with P. gingivalis proteases, the Arg- and Lys-gingipain proteases did not appear to be solely responsible for IL-8 attenuation. In addition, while P. gingivalis up-regulated IL-8 mRNA expression, this effect was overridden when the bacteria were continuously cocultured with the epithelial cells. The IL-8 mRNA levels in epithelial cells following sequential challenge with P. gingivalis andF. nucleatum and vice versa were approximately identical and were lower than those following F. nucleatum challenge alone and higher than control levels or those following P. gingivalis challenge alone. Thus, together with the protease effect, P. gingivalis possesses a powerful strategy to ensure the down-regulation of IL-8 and ICAM-1.

scholarly journals Lipopolysaccharide induces ICAM-1 expression via a c-Src/NADPH oxidase/ROS-dependent NF-κB pathway in human pulmonary alveolar epithelial cells

2016 ◽  
Vol 310 (7) ◽  
pp. L639-L657 ◽  
Author(s):  
Rou-Ling Cho ◽  
Chien-Chung Yang ◽  
I-Ta Lee ◽  
Chih-Chung Lin ◽  
Pei-Ling Chi ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Adhesion Molecule ◽  
Alveolar Epithelial Cells ◽  
Intercellular Adhesion Molecule ◽  
Ros Generation ◽  
Intercellular Adhesion Molecule 1 ◽  
Mapk Activation ◽  
Promoter Assay ◽  
Alveolar Epithelial

Upregulation of intercellular adhesion molecule-1 (ICAM-1) is frequently implicated in lung inflammation. Lipopolysaccharide (LPS) has been shown to play a key role in inflammation via adhesion molecule induction and then causes lung injury. However, the mechanisms underlying LPS-induced ICAM-1 expression in human pulmonary alveolar epithelial cells (HPAEpiCs) remain unclear. We showed that LPS induced ICAM-1 expression in HPAEpiCs, revealed by Western blotting, RT-PCR, real-time PCR, and promoter assay. Pretreatment with the inhibitor of c-Src (protein phosphatase-1, PP1), reactive oxygen species (ROS) (Edaravone), NADPH oxidase (apocynin and diphenyleneiodonium chloride), EGFR (AG1478), PDGFR (AG1296), phosphatidylinositol-3-kinase (PI3K) (LY294002), MEK1/2 (U0126), or NF-κB (Bay11-7082) and transfection with siRNAs of c-Src, EGFR, PDGFR, Akt, p47 phox, Nox2, Nox4, p42, and p65 markedly reduced LPS-induced ICAM-1 expression and monocyte adherence to HPAEpiCs challenged with LPS. In addition, we established that LPS stimulated phosphorylation of c-Src, EGFR, PDGFR, Akt, or p65, which was inhibited by pretreatment with their respective inhibitors. LPS induced Toll-like receptor 4 (TLR4), MyD88, TNF receptor-associated factor 6 (TRAF6), c-Src, p47 phox, and Rac1 complex formation 2, which was attenuated by transfection with c-Src or TRAF6 siRNA. Furthermore, LPS markedly enhanced NADPH oxidase activation and intracellular ROS generation, which were inhibited by PP1. We established that LPS induced p42/p44 MAPK activation via a c-Src/NADPH oxidase/ROS/EGFR, PDGFR/PI3K/Akt-dependent pathway in these cells. Finally, we observed that LPS significantly enhanced NF-κB and IκBα phosphorylation, NF-κB translocation, and NF-κB promoter activity, which were inhibited by PP1, Edaravone, apocynin, diphenyleneiodonium chloride, AG1478, AG1296, LY294002 , or U0126. These results demonstrated that LPS induces p42/p44 MAPK activation mediated through the TLR4/MyD88/TRAF6/c-Src/NADPH oxidase/ROS/EGFR, PDGFR/PI3K/Akt pathway, which in turn initiates the activation of NF-κB and ultimately induces ICAM-1 expression in HPAEpiCs.

Selective induction of intercellular adhesion molecule-1 by interferon-gamma in human airway epithelial cells

1992 ◽  
Vol 263 (1) ◽  
pp. L79-L87 ◽  
Author(s):  
D. C. Look ◽  
S. R. Rapp ◽  
B. T. Keller ◽  
M. J. Holtzman
Keyword(s):  
Epithelial Cells ◽  
Interferon Gamma ◽  
Adhesion Molecule ◽  
Airway Epithelial Cells ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Tnf Alpha ◽  
Mrna Levels ◽  
Intercellular Adhesion Molecule 1 ◽  
Ifn Gamma

To evaluate the factors controlling migration of leukocytes into pulmonary airway epithelium, we determined the biochemical mechanisms responsible for the regulation of intercellular adhesion molecule-1 (ICAM-1) expression on cultured monolayers of human tracheal epithelial cells (HTECs) or SV40 virus-transformed human bronchial epithelial cells (BEAS-2B). Validation experiments with human umbilical vein endothelial cells (HUVECs) demonstrated little detectable ICAM-1 expression on unstimulated cells or on cells incubated with interferon-gamma (IFN-gamma), but HUVEC monolayers responded to interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha) with significant increases in ICAM-1 and ICAM-1-dependent adherence of polymorphonuclear leukocytes (PMNs). HTEC monolayers also exhibited no significant basal ICAM-1 expression but, in contrast to HUVEC monolayers, had marked increases in ICAM-1 expression and ICAM-1-dependent PMN adherence only after incubation with IFN-gamma (and not after IL-1 beta or TNF-alpha) treatment. BEAS-2B cells also exhibited relatively selective IFN-gamma stimulation of ICAM-1 expression and ICAM-1-dependent PMN adherence but (like late passage HTEC) showed significant basal ICAM-1 expression. Differences in IFN-gamma effect on ICAM-1 levels between HUVEC and HTEC monolayers were not due to differences in number or responsiveness of IFN-gamma receptors, because both cell types exhibited a similar number of receptors and other IFN-gamma-dependent responses of HUVECs remained active. In all analyses, ICAM-1 mRNA levels correlated closely with detection of ICAM-1 on the cell surface.(ABSTRACT TRUNCATED AT 250 WORDS)

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