Effects of Influenza on Alveolar Macrophage Viability Are Dependent on Mouse Genetic Strain.
Effects of Influenza on Alveolar Macrophage Viability Are Dependent on Mouse Genetic Strain.
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DOI：
10.4049/jimmunol.1701406
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发表时间：
2018-07-01
期刊：
影响因子：
--
通讯作者：
Metzger DW
中科院分区：
文献类型：
--
作者：
Califano D;Furuya Y;Metzger DW
流感病毒后继发细菌合并感染对人类健康构成严重威胁。因此，了解这种易感性增加的免疫学原因具有重要的临床意义。流感引起的肺泡巨噬细胞改变已被证明是细菌重复感染易感性增加的一个主要原因。然而，造成这一现象的机制仍存在争议，特别是肺泡巨噬细胞是否因流感感染而耗尽，或者在感染后维持不变，但吞噬活性受到破坏。这里提供的数据通过表明任一机制在个体小鼠品系中可能存在差异而解决了这个问题。 BALB/c 小鼠感染甲型流感后，肺泡巨噬细胞水平出现 IFN-γ 依赖性显着降低，而 C57Bl/6 小鼠的肺泡巨噬细胞水平在整个流感感染过程中保持不变，尽管细胞表现出改变的表型，即 CD11b 表达上调。无论是用低剂量还是高剂量的流感病毒进行感染，都会观察到这些毒株差异。此外，感染 H1N1 A/California/04/2009 (CA04) 或 H1N1 A/PR8/1934 (PR8) 病毒株也产生了类似的结果。无论肺泡巨噬细胞活力如何，BALB/c 和 C57Bl/6 小鼠均表现出对流感后细菌感染的高度易感性。这些发现解决了文献中明显的不一致之处，确定了肺泡巨噬细胞对流感感染反应的小鼠品系依赖性差异，并最终可能有助于将小鼠模型转化为临床应用。
Secondary bacterial coinfections following influenza virus pose a serious threat to human health. Therefore, it is of significant clinical relevance to understand the immunological causes of this increased susceptibility. Influenza-induced alterations in alveolar macrophages have been shown to be a major underlying cause of the increased susceptibility to bacterial superinfection. However, the mechanisms responsible for this remain under debate, specifically, whether alveolar macrophages are depleted in response to influenza infection or are maintained post-infection, but with disrupted phagocytic activity. The data presented here resolves this issue by showing that either mechanism can differentially occur in individual mouse strains. BALB/c mice exhibited a dramatic IFN-γ-dependent reduction in levels of alveolar macrophages following infection with influenza A, whereas alveolar macrophage levels in C57Bl/6 mice were maintained throughout the course of influenza infection, although the cells displayed an altered phenotype, namely an upregulation in CD11b expression. These strain differences were observed regardless of whether infection was performed with low or high doses of influenza virus. Furthermore, infection with either the H1N1 A/California/04/2009 (CA04) or H1N1 A/PR8/1934 (PR8) virus strain yielded similar results. Regardless of alveolar macrophage viability, both BALB/c and C57Bl/6 mice showed a high level of susceptibility to post-influenza bacterial infection. These findings resolve the apparent inconsistencies in the literature, identify mouse strain-dependent differences in the alveolar macrophage response to influenza infection, and ultimately, may facilitate translation of the mouse model to clinical application.
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影响因子：
3.1
作者：
AUTENRIETH, IB;BEER, M;HEESEMANN, J
通讯作者：
HEESEMANN, J
影响因子：
8
作者：
Califano D;Furuya Y;Roberts S;Avram D;McKenzie ANJ;Metzger DW
通讯作者：
Metzger DW
影响因子：
5.8
作者：
Eichinger KM;Egaña L;Orend JG;Resetar E;Anderson KB;Patel R;Empey KM
通讯作者：
Empey KM
DOI：
10.1164/rccm.201012-2036oc
发表时间：
2011-07-15
影响因子：
24.7
作者：
Huang, Fang-Fang;Barnes, Peter F.;Shams, Homayoun
通讯作者：
Shams, Homayoun
影响因子：
2.6
作者：
Do Thi Thu Hang;Choi, Eun-Jin;Shin, Yeun-Kyung
通讯作者：
Shin, Yeun-Kyung