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暴露于白细胞介素-1、肿瘤坏死因子α和干扰素γ的神经细胞产生趋化因子及表达黏附分子的情况。

Chemokine production and adhesion molecule expression by neural cells exposed to IL-1, TNF alpha and interferon gamma.

作者信息

Chuluyan H E, Lang B J, Yoshimura T, Kenney J S, Issekutz A C

机构信息

Department of Pediatrics, Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.

出版信息

Life Sci. 1998;63(21):1939-52. doi: 10.1016/s0024-3205(98)00470-6.

Abstract

We investigated the effect of TNF alpha, IL-1alpha and IFN gamma on two neuroblastoma (NB) cell lines (SK-N-SH and SK-N-MC). These lines responded differentially to IL-1alpha, TNF alpha and IFN gamma for MCP-1 and IL-8 production and expression of the ICAM-1 and VCAM-1 adhesion molecules. None of the cytokines induced MCP-1 or IL-8 on SK-N-MC cells. Both chemokines were produced in response to IL-1alpha by SK-N-SH cells, while TNF alpha induced mainly MCP-1 production. Addition of IFN gamma decreased IL-8, but not MCP-1 production. These responses correlated with monocyte and neutrophil chemotactic activity in NB culture supernatants. This activity was neutralized by antibodies to IL-8 and MCP-1. The expression of ICAM-1 on SK-N-MC was up-regulated by TNF alpha or IFN gamma, while IL-1alpha also upregulated ICAM-1 on SK-N-SH cells. VCAM-1 expression on SK-N-SH was induced by IL-1alpha and TNF alpha and IFN gamma synergized with TNF alpha in this respect on both NB cell lines. These results suggest that mechanisms for chemokine production and VCAM-1 and ICAM-1 upregulation by inflammatory cytokines differ and IFN gamma, in conjunction with TNF alpha, stimulate neural cell responses (high MCP-1 and VCAM-1 and decreased IL-8) favouring mononuclear cell recruitment.

摘要

我们研究了肿瘤坏死因子α(TNFα)、白细胞介素-1α(IL-1α)和干扰素γ(IFNγ)对两种神经母细胞瘤(NB)细胞系(SK-N-SH和SK-N-MC)的影响。这些细胞系对IL-1α、TNFα和IFNγ在单核细胞趋化蛋白-1(MCP-1)和白细胞介素-8(IL-8)产生以及细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)黏附分子表达方面有不同反应。细胞因子均未在SK-N-MC细胞上诱导产生MCP-1或IL-8。SK-N-SH细胞对IL-1α产生这两种趋化因子,而TNFα主要诱导MCP-1产生。添加IFNγ可降低IL-8产生,但不影响MCP-1产生。这些反应与NB培养上清液中的单核细胞和中性粒细胞趋化活性相关。该活性可被抗IL-8和MCP-1抗体中和。TNFα或IFNγ上调SK-N-MC上ICAM-1的表达,而IL-1α也上调SK-N-SH细胞上的ICAM-1。IL-1α、TNFα和IFNγ诱导SK-N-SH上VCAM-1的表达,在这方面IFNγ与TNFα在两种NB细胞系上有协同作用。这些结果表明,炎症细胞因子产生趋化因子以及上调VCAM-1和ICAM-1的机制不同,IFNγ与TNFα共同刺激神经细胞反应(高MCP-1和VCAM-1以及降低的IL-8),有利于单核细胞募集。

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