Endacea Inc., Research Triangle Park, NC 27709-2076, USA.
Innate Immun. 2012 Jun;18(3):373-89. doi: 10.1177/1753425911411595. Epub 2011 Aug 23.
Yersinia pestis, a Gram-negative bacillus causing plague and Centers for Disease Control and Prevention (CDC) classified Category A pathogen, has high potential as a bioweapon. Lipopolysaccharide, a virulence factor for Y. pestis, binds to and activates A(1) adenosine receptor (AR)s and, in animals, A(1)AR antagonists block induced acute lung injury (ALI) and increase survival following cecal ligation and perforation. In this study, rats were infected intratracheally with viable Y. pestis [CO99 (pCD1( + )/Δpgm) 1 × 10( 8 ) CFU/animal] and treated daily for 3 d with ciprofloxacin (cipro), the A(1)AR antagonist L-97-1, or cipro plus L-97-1 starting at 0, 6, 24, 48, or 72 h post-Y. pestis. At 72 h post-Y. pestis, cipro plus L-97-1 significantly improved 6-d survival to 60-70% vs 28% for cipro plus H(2)O and 33% for untreated Y. pestis controls (P = 0.02, logrank test). Lung edema, hemorrhage and leukocyte infiltration index (LII) were evaluated histologically to produce ALI scores. Cipro plus L-97-1 significantly reduced lung edema, as well as aggregate lung injury scores vs controls or cipro plus H(2)O, and LII vs controls (P < 0.05, Student's unpaired t test). These results support efficacy for L-97-1 as a post-exposure medical countermeasure, adjunctive therapy to antibiotics for Y. pestis.
鼠疫耶尔森菌是一种革兰氏阴性杆菌,可引起鼠疫,被美国疾病控制与预防中心(CDC)归类为 A 类病原体,具有很高的生物武器潜力。鼠疫耶尔森菌的一种毒力因子——脂多糖,与 A(1) 腺苷受体(AR)结合并激活该受体,在动物中,A(1)AR 拮抗剂可阻断诱导性急性肺损伤(ALI),并在盲肠结扎穿孔后增加存活率。在这项研究中,大鼠通过气管内感染活的鼠疫耶尔森菌[CO99(pCD1( + )/Δpgm)1×10(8)CFU/动物],并用环丙沙星(cipro)、A(1)AR 拮抗剂 L-97-1 或 cipr o 加 L-97-1 每日治疗 3 天,从鼠疫耶尔森菌感染后 0、6、24、48 或 72 小时开始治疗。在感染鼠疫耶尔森菌后 72 小时,cipro 加 L-97-1 显著提高了 6 天的存活率,达到 60-70%,而 cipr o 加 H(2)O 组为 28%,未治疗的鼠疫耶尔森菌对照组为 33%(P=0.02,对数秩检验)。通过组织学评估肺水肿、出血和白细胞浸润指数(LII),以产生 ALI 评分。cipro 加 L-97-1 显著降低肺水肿,以及与对照组或 cipr o 加 H(2)O 相比的总肺损伤评分,以及与对照组相比的 LII(P<0.05,学生未配对 t 检验)。这些结果支持 L-97-1 作为暴露后医疗对策的有效性,作为鼠疫耶尔森菌抗生素的辅助治疗。