Adhesion of peripheral blood mononuclear cells and CD4+ T cells from patients with psoriasis to cultured endothelial cells via the interaction between lymphocyte function-associated antigen type 1 and intercellular adhesion molecule 1

Watabe, Daisuke; Kanno, Hiroyuki; Yoshida, Aki; Kurose, Akira; Akasaka, T; Sawai, Takashi

doi:10.1111/j.1365-2133.2007.08039.x

Cited by 19 publications

(16 citation statements)

References 41 publications

(98 reference statements)

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“…Previous studies have demonstrated that HMVECs have increased expression of select adhesion molecules induced by TNFα [28]. Cell surface ELISAs were performed to determine TNFα (25 ng/ml)-induced endothelial molecules implicated in angiogenesis - namely VCAM-1, ICAM-1, E-selectin, and JAM expression on HMVECs.…”

Section: Resultsmentioning

confidence: 99%

Suppression of endothelial cell activity by inhibition of tumor necrosis factor-alpha

et al. 2012

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IntroductionTNFα is a proinflammatory cytokine that plays a central role in the pathogenesis of rheumatoid arthritis (RA). We investigated the effects of certolizumab pegol, a TNFα blocker, on endothelial cell function and angiogenesis.MethodsHuman dermal microvascular endothelial cells (HMVECs) were stimulated with TNFα with or without certolizumab pegol. TNFα-induced adhesion molecule expression and angiogenic chemokine secretion were measured by cell surface ELISA and angiogenic chemokine ELISA, respectively. We also examined the effect of certolizumab pegol on TNFα-induced myeloid human promyelocytic leukemia (HL-60) cell adhesion to HMVECs, as well as blood vessels in RA synovial tissue using the Stamper-Woodruff assay. Lastly, we performed HMVEC chemotaxis, and tube formation.ResultsCertolizumab pegol significantly blocked TNFα-induced HMVEC cell surface angiogenic E-selectin, vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression and angiogenic chemokine secretion (P < 0.05). We found that certolizumab pegol significantly inhibited TNFα-induced HL-60 cell adhesion to HMVECs (P < 0.05), and blocked HL-60 cell adhesion to RA synovial tissue vasculature (P < 0.05). TNFα also enhanced HMVEC chemotaxis compared with the negative control group (P < 0.05) and this chemotactic response was significantly reduced by certolizumab pegol (P < 0.05). Certolizumab pegol inhibited TNFα-induced HMVEC tube formation on Matrigel (P < 0.05).ConclusionOur data support the hypothesis that certolizumab pegol inhibits TNFα-dependent leukocyte adhesion and angiogenesis, probably via inhibition of angiogenic adhesion molecule expression and angiogenic chemokine secretion.

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Section: Resultsmentioning

confidence: 99%

Suppression of endothelial cell activity by inhibition of tumor necrosis factor-alpha

et al. 2012

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“…Research demonstrates that the adhesion of CD4+ T cells to endothelial cells and the resulting migration to skin tissue are necessary in the development of psoriatic skin lesions. The adhesion molecules lymphocyte function associated antigen (LFA-1 or CD18) and ICAM-1 are key in the adhesion of CD4+ T cells to the endothelial wall (Watabe et al, 2007). Currently, both cell adhesion molecule antagonists and cytokine antagonists are approved for the treatment of psoriasis (Berger and Gottlieb, 2007).…”

Section: Discussionmentioning

confidence: 99%

Traditional herbal remedies that influence cell adhesion molecule activity

Spelman

Aldag

Hamman

et al. 2010

Phytotherapy Research

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Many traditional medicines have demonstrated immune activity, however, research has largely neglected their effects on cell adhesion molecules (CAMs). This review reports on extracts from 37 medicinal plant species, similar to or replicating traditional preparations, that up- or downregulate either gene or protein activity of CAMs. The majority of the investigations were in vitro, primarily of the immunoglobulin superfamily of CAMs, specifically intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and secondarily on the integrin (CD11b or MAC-1) and selectin (E-selectin and P-selectin) families of CAMs. The following plant species have demonstrated modulation of multiple CAMs: Artemisia asiatica, Boswellia serrata, Canscora decussata, Cinnamomum povectum, Dehaasia incrassate, Ganoderma lucidum, Ginkgo biloba, Hypericum perforatum, Juglans regia, Lycopus lucidus, Panax notoginseng, Rheum undulatum, Salvia miltiorrhiza. Many other species have documented activity on one CAM. Currently there are limited in vivo/ex vivo investigations, including a clinical trial on Mahonia aquifolium. Although further evidence is needed, the data suggest that the reviewed botanical medicines may have the potential to provide therapeutic potential in disease processes involving CAMs. Additionally, the reported success of many of these plant extracts by traditional cultures and modern phytotherapists may involve the modulation of CAMs.

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“…However, in some pathological conditions, such as in the inflammatory process, leukocyte accumulation can be amplified rapidly, which is an important pathogenic factor in tissue damage and the development of many types of pathologic inflammatory disorders, including inflammatory skin diseases (Charo and Ransohoff 2006). Human dermal microvascular endothelial cells, known as a selective barrier between the circulating blood and the vessel wall, are responsible for leukocyte migration into inflamed skin by the expression and secretion of adhesion molecules and chemokines (Swerlick and Lawley 1993;Watabe et al 2007). …”

Section: Introductionmentioning

confidence: 98%

Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

Cao

Chen

Guo

et al. 2014

Can. J. Physiol. Pharmacol.

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Monoammonim glycyrrhizate (MAG) derived from licorice has been shown to have anti-inflammatory properties. Chemokines are vital inflammatory mediators that are involved with endothelial damage from leukocyte infiltrates in various inflammatory skin diseases. In this study, we investigated the anti-inflammatory effects and mechanisms of MAG on tumor necrosis factor-α (TNF-α) induced chemokine production in a human dermal microvascular endothelial cell line (HMEC-1). HMEC-1 cells were treated with TNF-α, with or without MAG. The results showed that MAG suppressed TNF-α-induced chemokine (including CXCL8, CX3CL1, and CXCL16) mRNA expression in HMEC-1 cells, in a dose-dependent manner, and reduced the secretion of these chemokines in culture supernatant. Moreover, endothelial activation in the presence of MAG blocked the chemotactic activities of TNF-α-stimulated HMEC-1 cell supernatant on the migration of primary neutrophils and primary monocytes. In addition, Western blot and immunofluorescence data revealed that MAG inhibited nuclear translocation of nuclear factor-κB p65 (NF-κB p65). It is the first report to demonstrate that MAG suppresses TNF-α-induced chemokine production in HMEC-1 cells, and that the mechanism may be inhibiting the translocation of NF-κB p65 into the nucleus to prevent the starting of inflammatory signaling pathway. Our results revealed that MAG is a potential anti-inflammatory agent capable of improving inflammatory skin diseases.

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Adhesion of peripheral blood mononuclear cells and CD4+ T cells from patients with psoriasis to cultured endothelial cells via the interaction between lymphocyte function-associated antigen type 1 and intercellular adhesion molecule 1

Abstract: These findings indicate that the LFA-1/ICAM-1 interaction plays a major role in the adhesion of CD4+ T cells to endothelial cells and that TNF-alpha might play an important role for the induction of adhesion molecules on endothelial cells at psoriatic skin lesions.

Cited by 19 publications

References 41 publications

Suppression of endothelial cell activity by inhibition of tumor necrosis factor-alpha

Suppression of endothelial cell activity by inhibition of tumor necrosis factor-alpha

Traditional herbal remedies that influence cell adhesion molecule activity

Monoammonium glycyrrhizate suppresses tumor necrosis factor-α induced chemokine production in HMEC-1 cells, possibly by blocking the translocation of nuclear factor-κB into the nucleus

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