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联苯菊酯可激活人T细胞系中的同型聚集。

Bifenthrin activates homotypic aggregation in human T-cell lines.

作者信息

Hoffman Nataly, Tran Van, Daniyan Anthony, Ojugbele Olutosin, Pryor Stephen C, Bonventre Josephine A, Flynn Katherine, Weeks Benjamin S

机构信息

Department of Biology, Adelphi University, One South Avenue, Garden City, NY 11530, USA.

出版信息

Med Sci Monit. 2006 Mar;12(3):BR87-94. Epub 2006 Feb 23.

Abstract

BACKGROUND

Here, we addressed the concern that, despite the lack of overt toxicity, exposure to low levels of the common household pyrethroid pesticide, bifenthrin, could cause harm to the immune system. To do this, we measure the effect of bifenthrin on phytohemagglutinin (PHA) activation of homotypic aggregation in human T-cell lines.

MATERIAL/METHODS: The human CD4+ H9, and Jurkat cell lines and the human promonocyte U937 cell line, were exposed to varying concentrations of bifenthrin. Cell viability was determined using the AlmarBlue Toxicity Assay. Concentrations of bifenthrin which did not reduce cell viability were determined and these concentrations were tested for the effect of bifenthrin on PHA-mediated homotypic aggregation. Blocking antibodies to ICAM and LFA-1 were used to disrupt aggregation and a nonspecific IgG was used as a control.

RESULTS

Bifenthrin was found to be nontoxic at concentrations ranging from 10(-4) to 10(-13) M. Bifenthrin did not inhibit PHA induced cell aggregation in all cell lines tested. However, at 10(-4) M, bifenthrin to form aggregates stimulated homotypic aggregation in the H9 and Jurkat T-cell lines. The bifenthrin-induced aggregate formation, like that seen with PHA, was blocked by treating the cells with antibodies to either LFA-1 or ICAM.

CONCLUSIONS

The results here show that bifenthrin activates T-cell function by stimulating ICAM/LFA-1 mediated homotypic aggregation. This data suggests that exposure to bifenthrin, even at "acceptable" limits, can increase the risk for and frequency of inflammatory responses and diseases such as asthma.

摘要

背景

在此,我们探讨了一个问题,即尽管缺乏明显毒性,但接触低水平常见家用拟除虫菊酯农药联苯菊酯可能会对免疫系统造成损害。为此,我们测量了联苯菊酯对人T细胞系中植物血凝素(PHA)激活的同型聚集的影响。

材料/方法:将人CD4 + H9细胞系、Jurkat细胞系和人原单核细胞U937细胞系暴露于不同浓度的联苯菊酯中。使用AlmarBlue毒性测定法测定细胞活力。确定未降低细胞活力的联苯菊酯浓度,并测试这些浓度下联苯菊酯对PHA介导的同型聚集的影响。使用针对细胞间黏附分子(ICAM)和淋巴细胞功能相关抗原-1(LFA-1)的阻断抗体来破坏聚集,并使用非特异性IgG作为对照。

结果

发现联苯菊酯在10^(-4)至10^(-13) M的浓度范围内无毒。联苯菊酯在所有测试的细胞系中均未抑制PHA诱导的细胞聚集。然而,在10^(-4) M时,联苯菊酯在H9和Jurkat T细胞系中刺激同型聚集形成聚集体。联苯菊酯诱导的聚集体形成,与PHA诱导的情况一样,可通过用针对LFA-1或ICAM的抗体处理细胞来阻断。

结论

此处结果表明,联苯菊酯通过刺激ICAM/LFA-1介导的同型聚集来激活T细胞功能。该数据表明,即使在“可接受”的限度内接触联苯菊酯,也会增加炎症反应以及哮喘等疾病的风险和发生频率。

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