Constitutive expression of types 1 and 2 cytokines by alveolar macrophages from feline immunodeficiency virus-infected cats.

Constitutive expression of types 1 and 2 cytokines by alveolar macrophages from feline immunodeficiency virus-infected cats.
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DOI:
10.1016/s0165-2427(01)00250-1
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发表时间:
2001-05-10
影响因子:
1.8
通讯作者:
Tompkins MB
Tompkins MB
中科院分区:
农林科学3区
文献类型:
--
作者:
Ritchey JW;Levy JK;Bliss SK;Tompkins WA;Tompkins MB

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证据表明,猫免疫缺陷病毒(FIV),导致肺免疫缺陷。本研究的总体目的是探讨急性期感染期间fiv诱导肺间室细胞计数和细胞因子基因表达的改变。分别于fiv感染后0、4、10和16周收集fiv感染猫和对照猫的支气管肺泡灌洗(BAL)细胞进行表型和细胞因子分析。fiv感染后BAL细胞群的主要变化是中性粒细胞的发展。两组BAL细胞总数、肺泡巨噬细胞(AM)、嗜酸性粒细胞和淋巴细胞的相对数量保持相似。从BAL中纯化的AM的RT-qcPCR分析显示,TNFα、IL6和IL10 mrna的组成性表达在感染急性期达到峰值,然后下降。TNFα和il - 6生物活性蛋白的分泌也有类似的反应。相比之下,IFNγ的表达随着感染后的时间逐渐增加,并与AM中FIV-gag mRNA的逐渐增加相平行。il - 12 p40的表达也不同于其他细胞因子,在FIV感染后,AM - il - 12表达的猫的数量逐渐减少。体外感染FIV AM也会引起TNFα、IL6 mRNA和生物活性蛋白的增加,这表明FIV感染猫后AM细胞因子反应的增加是FIV感染AM的内在特征。总之,fiv感染的猫的肺部免疫变化与hiv感染的人类患者相似。
Evidence suggests that feline immunodeficiency virus (FIV), causes pulmonary immunodeficiency. The overall objective of this study was to explore FIV-induced alterations in cell counts and cytokine gene expression in the pulmonary compartment during the acute stage infection. Bronchoalveolar lavage (BAL) cells were collected from FIV-infected and control cats at 0, 4, 10, and 16 weeks post-FIV infection for phenotype and cytokine analysis. The major change in BAL cellular populations following FIV-infection was the development of a neutrophilia. Total BAL cell counts and relative numbers of alveolar macrophages (AM), eosinophils, and lymphocytes remained similar in both groups. The RT-qcPCR analyses of AM purified from BAL showed constitutive expression of TNFα, IL6 and IL10 mRNAs that peaked during the acute stage of infection then declined. The TNFα and IL6 bioactive protein secretion showed a similar response. In contrast, IFNγ expression increased progressively with time after infection and paralleled a progressive increase in FIV-gag mRNA in AM. The IL12 p40 expression also differed from the other cytokines in that there was a progressive decrease in the number of cats with AM IL12 expression following FIV infection. Infection of AM in vitro with FIV also caused an increase in TNFα and IL6 mRNA and bioactive protein suggesting that the increased cytokine response by AM following infection of cats with FIV is an intrinsic characteristic of FIV-infected AM. In summary, pulmonary immune changes seen in FIV-infected cats are similar to those seen in HIV-infected human patients.
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