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立克次氏体病原体通过色氨酸代谢物介导的p38丝裂原活化蛋白激酶激活来抑制蜱细胞死亡。

Rickettsial pathogen inhibits tick cell death through tryptophan metabolite mediated activation of p38 MAP kinase.

作者信息

Namjoshi Prachi, Dahmani Mustapha, Sultana Hameeda, Neelakanta Girish

机构信息

Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.

Department of Veterinary Medicine, University of Maryland-College Park, College Park, MD, USA.

出版信息

iScience. 2022 Dec 5;26(1):105730. doi: 10.1016/j.isci.2022.105730. eCollection 2023 Jan 20.

DOI:10.1016/j.isci.2022.105730
PMID:36582833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9792911/
Abstract

modulates various cell signaling pathways in mammalian cells for its survival. In this study, we report that . modulates tick tryptophan pathway to activate arthropod p38 MAP kinase for the survival of both this bacterium and its vector host. Increased level of tryptophan metabolite, xanthurenic acid (XA), was evident in . -infected ticks and tick cells. Lower levels of cell death markers and increased levels of total and phosphorylated p38 MAPK was noted in . -infected ticks and tick cells. Treatment with XA increased phosphorylated p38 MAPK levels and reduced cell death in . -infected tick cells. Furthermore, treatment with p38 MAPK inhibitor affected bacterial replication, decreased phosphorylated p38 MAPK levels and increased tick cell death. However, XA reversed these effects. Taken together, we provide evidence that rickettsial pathogen modulates arthropod tryptophan and p38 MAPK pathways to inhibit cell death for its survival in ticks.

摘要

为了生存,它可调节哺乳动物细胞中的各种细胞信号通路。在本研究中,我们报告称……调节蜱的色氨酸途径以激活节肢动物的p38丝裂原活化蛋白激酶,从而使这种细菌及其媒介宿主都得以生存。在……感染的蜱和蜱细胞中,色氨酸代谢产物黄尿酸(XA)水平升高是明显的。在……感染的蜱和蜱细胞中,细胞死亡标志物水平较低,总p38丝裂原活化蛋白激酶和磷酸化p38丝裂原活化蛋白激酶水平升高。用XA处理可增加磷酸化p38丝裂原活化蛋白激酶水平,并减少……感染的蜱细胞中的细胞死亡。此外,用p38丝裂原活化蛋白激酶抑制剂处理会影响细菌复制,降低磷酸化p38丝裂原活化蛋白激酶水平,并增加蜱细胞死亡。然而,XA可逆转这些作用。综上所述,我们提供的证据表明,立克次氏体病原体调节节肢动物的色氨酸和p38丝裂原活化蛋白激酶途径以抑制细胞死亡,从而在蜱中生存。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/858a2055ddea/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/5f3c520e9549/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/29a1560c8c24/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/aa4d8d39750f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/ef8f4509937f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/73e41f7ad4cd/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/285a8b27af16/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/c80f8678b58f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/858a2055ddea/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/5f3c520e9549/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/29a1560c8c24/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/aa4d8d39750f/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/ef8f4509937f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/73e41f7ad4cd/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/285a8b27af16/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/c80f8678b58f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a16e/9792911/858a2055ddea/gr7.jpg

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