Immortalized MH-S cells lack defining features of primary alveolar macrophages and do not support mouse pneumovirus replication.
Immortalized MH-S cells lack defining features of primary alveolar macrophages and do not support mouse pneumovirus replication.
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DOI：
10.1016/j.imlet.2016.02.012
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发表时间：
2016-04
影响因子：
4.4
通讯作者：
Rosenberg HF
中科院分区：
文献类型：
--
作者：
Brenner TA;Rice TA;Anderson ED;Percopo CM;Rosenberg HF
sv -40转化的h - s细胞系保持了BALB/c小鼠原代肺泡巨噬细胞（AMs）的部分特征，但不是全部特征。我们在这里发现，MH-S细胞在革兰氏阳性罗伊氏乳杆菌的攻击下，分别产生炎症细胞因子IL-6和CXCL10，以及TLR2和NOD2配体Pam3CSK4和MDP。相比之下，尽管野生型AMs在体内被小鼠肺炎病毒（PVM）感染，但在MH-S细胞中未检测到病毒复制。有趣的是，hh - s细胞的表面免疫表型（CD11c+Siglec F−）不同于野生型AMs (CD11c+Siglec F+)，与从粒细胞巨噬细胞集落刺激因子（GM-CSF）基因缺失小鼠中分离的未成熟AMs相似；GM-CSF−/−小鼠的AMs也支持PVM复制。然而，MH-S细胞不表达GM-CSF受体α链（CD116），对GM-CSF无应答。由于这些不寻常的特征，MH-S细胞作为AMs的实验模型应谨慎使用。
The SV-40-transformed MH-S cell line maintains some, but not all, features of primary alveolar macrophages (AMs) from BALB/c mice. We show here that MH-S cells produce inflammatory cytokines IL-6 and CXCL10 in response to challenge with Gram-positive Lactobacillus reuteri, and to TLR2 and NOD2 ligands Pam3CSK4 and MDP, respectively. In contrast, although wild-type AMs are infected in vivo by pneumonia virus of mice (PVM), no virus replication was detected in MH-S cells. Interestingly, the surface immunophenotype of MH-S cells (CD11c+Siglec F−) differs from that of wild-type AMs (CD11c+ Siglec F+) and is similar to that of immature AMs isolated from granulocyte macrophage-colony stimulating factor (GM-CSF) gene-deleted mice; AMs from GM-CSF−/− mice also support PVM replication. However, MH-S cells do not express the GM-CSF receptor alpha chain (CD116) and do not respond to GM-CSF. Due to these unusual features, MH-S cells should be used with caution as experimental models of AMs.