Neutropenia exacerbates infection by Acinetobacter baumannii clinical isolates in a murine wound model.
Neutropenia exacerbates infection by Acinetobacter baumannii clinical isolates in a murine wound model.
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DOI：
10.3389/fmicb.2015.01134
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发表时间：
2015
影响因子：
5.2
通讯作者：
Martinez LR
中科院分区：
文献类型：
--
作者：
Grguric-Smith LM;Lee HH;Gandhi JA;Brennan MB;DeLeon-Rodriguez CM;Coelho C;Han G;Martinez LR
近年来，革兰氏阴性球杆菌鲍曼不动杆菌已成为医院获得性感染的一个日益普遍的原因。临床上大多数A.鲍曼不动杆菌分离株显示出对抗菌剂的高水平耐药性，这严重损害了我们护理鲍曼不动杆菌患者的能力。鲍曼氏病。中性粒细胞在宿主防御微生物感染中具有重要作用。然而，这些天然免疫细胞在宿主抵抗皮肤A.鲍氏杆菌感染尚未进行直接调查。因此，我们假设中性粒细胞的耗竭增加了实验性A.鲍曼氏鼠创伤模型。本研究用Ly-6 G特异性单克隆抗体1A 8制备了A.研究了创伤皮肤组织上的鲍曼不动杆菌临床分离株。我们证明，中性粒细胞耗竭增加细菌负荷使用集落形成单位测定。此外，mAb 1A 8降低了A.感染鲍曼不动杆菌的动物有趣的是，从A.用mAb 1A 8处理的鲍曼不动杆菌感染的动物显示出增强的胶原沉积。此外，中性粒细胞减少症和A.鲍曼不动杆菌感染改变促炎细胞因子释放，导致严重的微生物疾病。我们的研究结果使我们更好地了解这些先天免疫细胞在控制A中的影响。鲍氏皮肤感染。
The Gram negative coccobacillus Acinetobacter baumannii has become an increasingly prevalent cause of hospital-acquired infections in recent years. The majority of clinical A. baumannii isolates display high-level resistance to antimicrobials, which severely compromises our capacity to care for patients with A. baumannii disease. Neutrophils are of major importance in the host defense against microbial infections. However, the contribution of these cells of innate immunity in host resistance to cutaneous A. baumannii infection has not been directly investigated. Hence, we hypothesized that depletion of neutrophils increases severity of bacterial disease in an experimental A. baumannii murine wound model. In this study, the Ly-6G-specific monoclonal antibody (mAb), 1A8, was used to generate neutropenic mice and the pathogenesis of several A. baumannii clinical isolates on wounded cutaneous tissue was investigated. We demonstrated that neutrophil depletion enhances bacterial burden using colony forming unit determinations. Also, mAb 1A8 reduces global measurements of wound healing in A. baumannii-infected animals. Interestingly, histological analysis of cutaneous tissue excised from A. baumannii-infected animals treated with mAb 1A8 displays enhanced collagen deposition. Furthermore, neutropenia and A. baumannii infection alter pro-inflammatory cytokine release leading to severe microbial disease. Our findings provide a better understanding of the impact of these innate immune cells in controlling A. baumannii skin infections.