Intranasal priming of newborn mice with microbial extracts increases opsonic factors and mature CD11c+ cells in the airway
Intranasal priming of newborn mice with microbial extracts increases opsonic factors and mature CD11c+ cells in the airway
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DOI：
10.1152/ajplung.00031.2012
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发表时间：
2012-11-01
影响因子：
4.9
通讯作者：
Kita, Eiji
中科院分区：
文献类型：
--
作者：
Kasahara, Kazuki;Matsumura, Yoko;Kita, Eiji
[10]李文，李文.用微生物提取物鼻内激发新生小鼠增加气道中的调理因子和成熟CD 11 c+细胞。Am J Physiol Lung Cell Mol Physiol 303：L834-L843，2012.首次发表于2012年8月24日; doi：10.1152/ajplung.00031.2012.-断奶后鼻暴露于微生物提取物混合物（MME）增强了新生小鼠对肺炎链球菌的气道阻力（J Physiol Lung Cell Mol Physiol 298：L 67，2010）。本研究旨在阐明致新生小鼠气道先天性阻力增强的有效因素。MME暴露显著增加气道中肺表面活性物质（SP-A和SP-D）的量。暴露小鼠的支气管肺泡灌洗液表现出更高水平的调理素活性，从而增强肺泡巨噬细胞（M空集）对S.肺炎。暴露本身并不增加气道中的补体成分C3和甘露聚糖结合凝集素A（MBL-A），而气道内感染S。与对照组小鼠相比，肺炎克雷伯氏菌暴露小鼠中SP-A、SP-D、C3和MBL-A的量显著增加。暴露增强了肺泡M空集上具有胶原结构的A类清道夫M空集受体的表达，并且还增加了肺中主要组织相容性复合物II+ CD 11 c+细胞的频率;这些细胞能够在体外产生IL-10和转化生长因子β。这些结果提示，早期暴露于微生物可增加新生小鼠气道中SP-A和SP-D的含量，增加清道夫M空集的数量，并促进CD 11 c+细胞的成熟，这可能与新生小鼠气道对S.肺炎。
Kasahara K, Matsumura Y, Ui K, Kasahara K, Komatsu Y, Mikasa K, Kita E. Intranasal priming of newborn mice with microbial extracts increases opsonic factors and mature CD11c+ cells in the airway. Am J Physiol Lung Cell Mol Physiol 303: L834-L843, 2012. First published August 24, 2012; doi:10.1152/ajplung.00031.2012.-Nasal exposure to the mixture of microbial extracts (MME) after ablactation enhanced airway resistance of newborn mice to Streptococcus pneumoniae (J Physiol Lung Cell Mol Physiol 298: L67, 2010). The present study was addressed to elucidate effective factors responsible for the enhanced innate resistance in the airway of MME-exposed newborn mice. MME exposure significantly increased the amount of pulmonary surfactants (SP-A and SP-D) in the airway. Bronchoalveolar lavage fluid of the exposed mice exhibited greater levels of opsonic activity, thereby enhancing the phagocytic and intracellular killing activities of alveolar macrophages (Mempty set) against S. pneumoniae. The exposure itself did not increase a complement component C3 and mannan-binding lectin-A (MBL-A) in the airway, whereas intratracheal infection with S. pneumoniae increased the quantity of SP-A, SP-D, C3, and MBL-A in the exposed mice to a significant extent compared with control mice. The exposure enhanced the expression of the class A scavenger Mempty set receptor with collagenous structure on alveolar Mempty set and also increased the frequency of major histocompatibility complex II+ CD11c+ cells in the lung; the cells were able to produce IL-10 and transforming growth factor-beta in vitro. These results suggest that microbial exposure early in life increases the amounts of SP-A and SP-D and the number of scavenger Mempty set and also promotes maturation of CD11c+ cells in the airway of newborn mice, which may be involved in airway resistance to S. pneumoniae.