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Cigarette smoke suppresses Th1 cytokine production and increases RSV expression in a neonatal model.

机译:在新生儿模型中,香烟烟雾抑制Th1细胞因子的产生并增加RSV表达。

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Respiratory syncytial virus (RSV) infects approximately 90% of young children by the age of 2 yr, with peak rates occurring during 2-6 mo of age. Exposure to side-stream cigarette smoke (SS) may increase the incidence or manifestation of an RSV infection. We hypothesized that exposure to SS would alter the subsequent immune response to RSV infection in neonatal mice. BALB/c mice were exposed to air or 1.5 mg/m3 of SS from day (d) 1 up to 35 d of age. A subset was intranasally infected with 4x10(4) PFU of RSV/g body wt on d 7 and rechallenged at 28 d of age. Immune responses were assessed on d 4 and 7 after RSV rechallenge. Both air- and SS-exposed mice responded to RSV rechallenge with neutrophilia and decreased Clara cell secretory protein levels within the lung. However, an increase in bronchoalveolar lavage fluid eosinophils, in addition to reduced levels of Th1 cytokines (IFN-gamma and IL-12), decreased lung tissue inflammation, and decreased mucus production was observed in SS-exposed mice compared with air-exposed mice after RSV rechallenge. Ultimately changes in cytokine and inflammatory responses due to SS exposure likely contributed to increased viral gene expression. These results suggest that SS exposure plays a significant role in shaping the neonatal response to RSV infection.
机译:到2岁时,呼吸道合胞病毒(RSV)感染约90%的年幼儿童,其最高发病率发生在2-6个月的年龄。接触侧流香烟烟雾(SS)可能会增加RSV感染的发生率或表现。我们假设接触SS将改变新生小鼠随后对RSV感染的免疫反应。从第(d)天第1天到35天,将BALB / c小鼠暴露于空气或1.5 mg / m3的SS中。在第7天,亚组鼻腔感染4x10(4)PFU的RSV / g体重,在28 d时再次受到感染。 RSV再攻击后第4和7天评估免疫反应。暴露于空气和暴露于SS的小鼠均对嗜中性粒细胞增多的RSV再攻击产生反应,并降低了肺内Clara细胞分泌蛋白的水平。但是,与暴露于空气的小鼠相比,暴露于SS的小鼠中除Th1细胞因子(IFN-γ和IL-12)水平降低,肺组织炎症降低和粘液生成减少外,支气管肺泡灌洗液嗜酸性粒细胞增多RSV再挑战之后。最终由于SS暴露而引起的细胞因子和炎性反应的改变可能导致病毒基因表达增加。这些结果表明,SS暴露在影响新生儿对RSV感染的反应中起着重要作用。

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