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模拟吸入性炭疽的宿主反应。

Modeling the host response to inhalation anthrax.

机构信息

Mathematical Biosciences Institute, 3rd Floor Jennings Hall, The Ohio State University, Columbus, OH 43210, USA.

出版信息

J Theor Biol. 2011 May 7;276(1):199-208. doi: 10.1016/j.jtbi.2011.01.054. Epub 2011 Feb 3.

DOI:10.1016/j.jtbi.2011.01.054
PMID:21295589
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3253853/
Abstract

Inhalation anthrax, an often fatal infection, is initiated by endospores of the bacterium Bacillus anthracis, which are introduced into the lung. To better understand the pathogenesis of an inhalation anthrax infection, we propose a two-compartment mathematical model that takes into account the documented early events of such an infection. Anthrax spores, once inhaled, are readily taken up by alveolar phagocytes, which then migrate rather quickly out of the lung and into the thoracic/mediastinal lymph nodes. En route, these spores germinate to become vegetative bacteria. In the lymph nodes, the bacteria kill the host cells and are released into the extracellular environment where they can be disseminated into the blood stream and grow to a very high level, often resulting in the death of the infected person. Using this framework as the basis of our model, we explore the probability of survival of an infected individual. This is dependent on several factors, such as the rate of migration and germination events and treatment with antibiotics.

摘要

吸入性炭疽,一种常致命的感染,是由炭疽杆菌的内生孢子引发的,这些内生孢子被引入肺部。为了更好地理解吸入性炭疽感染的发病机制,我们提出了一个两室数学模型,该模型考虑了这种感染的已记录的早期事件。一旦吸入炭疽孢子,它们就很容易被肺泡吞噬细胞摄取,然后迅速从肺部迁移到胸/纵隔淋巴结。在此过程中,这些孢子发芽成为营养细菌。在淋巴结中,细菌杀死宿主细胞并被释放到细胞外环境中,在那里它们可以传播到血液中并大量生长,通常导致感染者死亡。我们的模型以此框架为基础,探索了受感染者存活的概率。这取决于几个因素,如迁移和发芽事件的速度以及抗生素治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/5fd624ec4a13/nihms278699f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/33fe4ca9161f/nihms278699f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/fcf4e58a9d33/nihms278699f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/7c1bb36cec16/nihms278699f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/880b4d787e70/nihms278699f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/5fd624ec4a13/nihms278699f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/33fe4ca9161f/nihms278699f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/fcf4e58a9d33/nihms278699f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/7c1bb36cec16/nihms278699f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/880b4d787e70/nihms278699f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4810/3253853/5fd624ec4a13/nihms278699f5.jpg

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Anthrax lethal toxin and Salmonella elicit the common cell death pathway of caspase-1-dependent pyroptosis via distinct mechanisms.炭疽致死毒素和沙门氏菌通过不同机制引发依赖半胱天冬酶-1的细胞焦亡这一共同细胞死亡途径。
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