Interferon-γ influences the composition of leukocytic infiltrates in murine lyme carditis.

Interferon-γ influences the composition of leukocytic infiltrates in murine lyme carditis.
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干扰素-γ 影响小鼠莱姆病心脏炎白细胞浸润的组成。

DOI:
10.1016/j.ajpath.2011.06.029
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发表时间:
2011
期刊:
The American journal of pathology
影响因子:
--
通讯作者:
Furie,MarthaB
Furie,MarthaB
中科院分区:
--
文献类型:
--
作者:
Sabino,GregoryJ;Hwang,SonyaJ;McAllister,ShaneC;Mena,Patricio;Furie,MarthaB

文献摘要

相似文献

干扰素(IFN)-γ存在于莱姆病患者的病变中,并与症状的严重程度呈正相关。为了研究IFNγ在莱姆病发生中的作用,我们将野生型和IFNγ缺乏的C57BL/6小鼠感染了伯氏疏螺旋体。组织学分析显示,感染后14、21、25和28天,野生型和ifn γ-缺陷小鼠的心炎严重程度没有变化。然而,在25天观察到ifn - γ缺乏小鼠心脏内白细胞类型的明显变化。在缺乏IFNγ的情况下,心脏中性粒细胞的数量增加,而T淋巴细胞的数量减少。心脏内的细菌负荷与野生型小鼠相同。巨噬细胞分泌募集免疫细胞的趋化因子,这可能有助于小鼠莱姆病中白细胞的积累。IFNγ和b。研究发现,这两种刺激可协同诱导单核细胞(CXCL9、CXCL10、CXCL11、CXCL16和CCL12)的趋化剂,并降低中性粒细胞(CXCL1、CXCL2和CXCL3)的趋化剂。干扰素γandB。burgdorferi还能协同增强小鼠心脏内皮细胞CXCL9和CXCL10的分泌。这些结果表明,IFNγ通过促进与慢性炎症相关的白细胞的积累和抑制典型急性炎症的细胞的积累,影响莱姆病中炎症浸润的组成。
Interferon (IFN)-γ is present in lesions of patients with Lyme disease and positively correlates with the severity of manifestations. To investigate the role of IFNγ in the development of Lyme carditis, wild-type and IFNγ-deficient C57BL/6 mice were infected with the causative bacterium,Borrelia burgdorferi. Histological analysis revealed no change in the severity of carditis between wild-type and IFNγ-deficient mice at 14, 21, 25, and 28 days after infection. However, a distinct shift in the types of leukocytes within the hearts of IFNγ-deficient mice was observed at 25 days. In the absence of IFNγ, the number of neutrophils in the heart was increased, whereas the number of T lymphocytes was decreased. Bacterial loads within hearts were the same as in wild-type mice. Macrophages secrete chemokines that recruit immune cells, which could contribute to the accumulation of leukocytes in murine Lyme carditis. The ability of IFNγ andB. burgdorferito activate murine macrophages was examined, and the two stimuli synergistically induced chemoattractants for mononuclear cells (ie, CXCL9, CXCL10, CXCL11, CXCL16, and CCL12) and decreased those for neutrophils (ie, CXCL1, CXCL2, and CXCL3). IFNγ andB. burgdorferialso synergistically enhanced secretion of CXCL9 and CXCL10 by murine cardiac endothelial cells. These results indicate that IFNγ influences the composition of inflammatory infiltrates in Lyme carditis by promoting the accumulation of leukocytes associated with chronic inflammation and suppressing that of cells that typify acute inflammation.