Teunis Allison L, Popova Taissia G, Espina Virginia, Liotta Lance A, Popov Serguei G
Department of Molecular Microbiology, National Center for Biodefense and Infectious Diseases, School of Systems Biology, George Mason UniversityManassas, VA, United States.
Department of Molecular Microbiology, Center for Applied Proteomics and Molecular Medicine, School of Systems Biology, George Mason UniversityManassas, VA, United States.
Front Mol Biosci. 2017 Aug 28;4:62. doi: 10.3389/fmolb.2017.00062. eCollection 2017.
We recently reported that the open-mesh (0.7 μ) polyacrylamide microparticles (MPs) with internally-coupled Cibacron affinity dye demonstrate protective effect in mice challenged into footpads with high doses (200 LD50) of anthrax (Sterne) spores. A single injection of MPs before spore challenge reduces inflammatory response, delays onset of mortality and promotes survival. In this study, we show that the effect of MPs was substantially increased at the lower spore dose (7 LD50). The inflammation of footpads was reduced to the background level, and 60% of animals survived for 16 days while all untreated infected animals died within 6 days with strong inflammation. The effects of MPs were promoted when the MPs were loaded with a combination of neutrophil-attracting chemokines IL-8 and MIP-1α which delayed the onset of mortality in comparison with untreated mice for additional 8 days. The MPs were not inherently cytotoxic against the bacteria or cultured murine Raw 264.7 cells, but stimulated these cells to release G-CSF, MCP-1, MIP-1α, and TNF-α. Consistent with this finding the injection of MPs induced neutrophil influx into footpads, stimulated production of TNF-α associated with migration of pERK1/2-positive cells with the Langerhans phenotype from epidermis to regional lymph nodes. Our data support the mechanism of protection in which the immune defense induced by MPs along with the exogenous chemokines counterbalances the suppressive effect caused by anthrax infection.
我们最近报道,具有内部偶联汽巴克隆亲和染料的开放网格(0.7微米)聚丙烯酰胺微粒(MPs)在经高剂量(200 LD50)炭疽(斯特恩)孢子攻击足垫的小鼠中显示出保护作用。在孢子攻击前单次注射MPs可减轻炎症反应、延迟死亡 onset 并提高存活率。在本研究中,我们表明在较低孢子剂量(7 LD50)下,MPs的效果显著增强。足垫炎症减轻至背景水平,60%的动物存活16天,而所有未治疗的感染动物在6天内死亡且伴有强烈炎症。当MPs负载吸引中性粒细胞的趋化因子IL-8和MIP-1α的组合时,MPs的效果得到增强,与未治疗的小鼠相比,这延迟了死亡 onset 达8天。MPs本身对细菌或培养的小鼠Raw 264.7细胞无细胞毒性,但刺激这些细胞释放G-CSF、MCP-1、MIP-1α和TNF-α。与此发现一致,注射MPs可诱导中性粒细胞流入足垫,刺激TNF-α的产生,这与具有朗格汉斯表型的pERK1/2阳性细胞从表皮迁移至区域淋巴结有关。我们的数据支持这样一种保护机制,即MPs与外源性趋化因子诱导的免疫防御可抵消炭疽感染引起的抑制作用。