Roux Damien, Weatherholt Molly, Clark Bradley, Gadjeva Mihaela, Renaud Diane, Scott David, Skurnik David, Priebe Gregory P, Pier Gerald, Gerard Craig, Yoder-Himes Deborah R
IAME, UMR 1137, INSERM, Université Paris Diderot, Sorbonne Paris Cité, Service de Réanimation médico-chirurgicale, Hôpital Louis Mourier, AP-HP, Colombes, France.
Department of Biology, University of Louisville, Louisville, Kentucky, USA.
Infect Immun. 2017 May 23;85(6). doi: 10.1128/IAI.00765-16. Print 2017 Jun.
caused an outbreak in the cystic fibrosis (CF) clinic at Boston Children's Hospital from 1998 to 2005 and led to the infection of over 40 patients, many of whom died due to complications from infection by this organism. To assess whether significantly contributes to disease or is recognized by the host immune response, mice were infected with a sequenced outbreak strain, AU0158, and responses were compared to those to the well-studied CF pathogen In parallel, mice were also infected with a polar flagellin mutant of to examine the role of flagella in lung colonization. The results showed a higher persistence in the host by strains, and yet, neutrophil recruitment and cytokine production were lower than those with The ability of host immune cells to recognize was then assessed, induced a robust cytokine response in cultured cells, and this effect was dependent on the flagella only when bacteria were dead. Together, these results suggest that can be recognized by host cells but may avoid or suppress the host immune response through unknown mechanisms. was then compared to other species and found to induce similar levels of cytokine production despite being internalized by macrophages more than strains. These data suggest that AU0158 may act differently with host cells and is recognized differently by immune systems than are other strains or species.
1998年至2005年期间,在波士顿儿童医院的囊性纤维化(CF)诊所引发了一次疫情,导致40多名患者感染,其中许多患者因感染这种病原体引发的并发症而死亡。为了评估[病原体名称]是否对疾病有显著影响或是否能被宿主免疫反应识别,用一株测序的疫情爆发菌株AU0158感染小鼠,并将其反应与对研究充分的CF病原体[另一病原体名称]的反应进行比较。同时,还用[病原体名称]的极性鞭毛蛋白突变体感染小鼠,以研究鞭毛在肺部定植中的作用。结果显示,[病原体名称]菌株在宿主中的持续存在时间更长,然而,中性粒细胞募集和细胞因子产生低于[另一病原体名称]。随后评估宿主免疫细胞识别[病原体名称]的能力,[病原体名称]在培养细胞中诱导了强烈的细胞因子反应,并且只有当细菌死亡时,这种效应才依赖于鞭毛。综合这些结果表明,[病原体名称]可被宿主细胞识别,但可能通过未知机制避免或抑制宿主免疫反应。然后将[病原体名称]与其他[病原体名称]物种进行比较,发现尽管[病原体名称]被巨噬细胞内化的程度高于[其他病原体名称]菌株,但它们诱导的细胞因子产生水平相似。这些数据表明,[病原体名称]AU0158与宿主细胞的相互作用可能不同,并且与其他[病原体名称]菌株或物种相比,其被免疫系统识别的方式也不同。