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Caenorhabditis elegans mounts a p38 MAPK pathway-mediated defence to Cutibacterium acnes infection.
Cellular Microbiology ( IF 3.4 ) Pub Date : 2020-06-15 , DOI: 10.1111/cmi.13234
Xiaowen Huang 1, 2 , Wen Pan 2 , Wooseong Kim 3 , Alexis White 2, 4 , Silei Li 2 , Huiying Li 5, 6 , Kiho Lee 2 , Beth Burgwyn Fuchs 2 , Kang Zeng 1 , Eleftherios Mylonakis 2
Affiliation  

Cutibacterium acnes is capable of inducing inflammation in acne and can lead to a chronic prostatic infection. The diverse pathogenicity among different strains of C. acnes has been presented, but simple appropriate animal models for the evaluation of this bacterium are lacking. In this study, the nematode Caenorhabditis elegans was used as an invertebrate infection model. We revealed that C. acnes type strain ATCC 6919 caused lethal infections to C. elegans in solid and liquid culture media (p < .0001). Compared with the strain ATCC 6919, the antibiotic‐resistant strain HM‐513 was more virulent, resulting in reduced survival (p < .0001). Four different C. acnes strains killed worms with a p value of less than .0001 when provided to C. elegans at 4.8 × 108 CFU/ml. The infection model was also employed to explore host defence responses. An increase in numerous immune effectors in response to C. acnes was detected. We focused on nine C‐type lectins, including: clec‐13, clec‐17, clec‐47, clec‐52, clec‐60, clec‐61, clec‐70, clec‐71 and clec‐227. The induced expression of these C‐type lectin genes was down‐regulated in mutant worms deficient in the p38 mitogen‐activated protein kinase (MAPK) pathway. Meanwhile, PMK‐1 (MAPK) was phosphorylated and activated at the onset of C. acnes infection. By monitoring the survival of mutant worms, we found that PMK‐1, SEK‐1 (MAPKK) and TIR‐1 (MAPKKK) were critical in responding to C. acnes infection. C. elegans pmk‐1 and tir‐1 mutants exhibited higher mortality to C. acnes infection (p < .0001). In conclusion, C. elegans serves as a simple and valuable model to study C. acnes virulence and facilitates improvements in understanding of host innate immune responses.

中文翻译:

秀丽隐杆线虫启动 p38 MAPK 通路介导的对痤疮皮肤杆菌感染的防御。

痤疮皮肤杆菌能够引起痤疮炎症,并可能导致慢性前列腺感染。痤疮丙酸杆菌不同菌株之间的不同致病性已被提出,但缺乏用于评估这种细菌的简单、适当的动物模型。在这项研究中,线虫秀丽隐杆线虫被用作无脊椎动物感染模型。我们发现C.acnes型菌株 ATCC 6919在固体和液体培养基中对C. elegans造成致命感染( p  < .0001)。与菌株 ATCC 6919 相比,抗生素抗性菌株 HM-513 的毒性更强,导致存活率降低 ( p  < .0001)。四种不同当以 4.8 × 10 8  CFU/ml提供给C. elegans时,痤疮 C.菌株杀死了p值小于 0.0001 的蠕虫。感染模型也被用来探索宿主防御反应。检测到响应于痤疮丙酸杆菌的许多免疫效应物增加。我们专注于九种 C 型凝集素,包括:clec-13clec-17clec-47clec-52clec-60clec-61clec-70clec-71clec-227. 这些 C 型凝集素基因的诱导表达在 p38 丝裂原活化蛋白激酶 (MAPK) 途径缺陷的突变蠕虫中被下调。同时,PMK-1(MAPK)在痤疮丙酸杆菌感染开始时被磷酸化和激活。通过监测突变蠕虫的存活情况,我们发现 PMK-1、SEK-1 (MAPKK) 和 TIR-1 (MAPKKK) 对响应痤疮丙酸杆菌感染至关重要。线虫PMK-1TIR-1到突变体显示出较高的死亡率C.痤疮丙酸杆菌感染(p  <0.0001)。总之,C. elegans是研究C.acnes 的一个简单而有价值的模型 毒力并促进对宿主先天免疫反应的理解。
更新日期:2020-06-15
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