Finding Order in the Chaos: Outstanding Questions in Klebsiella pneumoniae Pathogenesis.
Finding Order in the Chaos: Outstanding Questions in Klebsiella pneumoniae Pathogenesis.
复制标题
在混乱中找到秩序：克雷伯氏菌发病机理中的杰出问题。
DOI：
10.1128/iai.00693-20
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发表时间：
2021-03-17
影响因子：
3.1
通讯作者：
Van Tyne D
中科院分区：
文献类型：
--
作者：
Gonzalez-Ferrer S;Peñaloza HF;Budnick JA;Bain WG;Nordstrom HR;Lee JS;Van Tyne D
肺炎克雷伯氏菌是革兰氏阴性兼性厌氧菌，存在于宿主相关的肠道微生物组中，但它们也可以引起广泛的感染，这些感染通常难以治疗。肺炎，称为经典或高毒力菌株。肺炎克雷伯氏菌是革兰氏阴性兼性厌氧菌，存在于宿主相关的肠道微生物组中，但它们也可以引起广泛的感染，这些感染通常难以治疗。肺炎，称为经典或高毒力菌株。这两个群体在遗传上是不同的，居住在不重叠的地理区域，并在人类中引起不同类型的有害感染。这些不同的细菌群体也被发现与宿主免疫系统有不同的相互作用。初始先天免疫防御K。肺炎链球菌感染的免疫系统包括补体、巨噬细胞、嗜中性粒细胞和单核细胞;这些防御是宿主清除感染的主要策略。K.肺炎的发病机制取决于微生物和这些宿主防御中的每一种之间的相互作用，并且细菌遗传多样性影响这些相互作用的结果变得越来越明显。在这里，我们强调了我们对K的理解的最新进展。pneumoniae的发病机制，重点是细菌进化和多样性如何影响K.肺炎与哺乳动物先天免疫宿主防御的相互作用。我们还讨论了悬而未决的问题，如何K。肺炎可以破坏正常的免疫应答，利用免疫妥协状态，并引起高死亡率的感染。
Klebsiella pneumoniae are Gram-negative facultative anaerobes that are found within host-associated commensal microbiomes, but they can also cause a wide range of infections that are often difficult to treat. These infections are caused by different pathotypes of K. pneumoniae, called either classical or hypervirulent strains. Klebsiella pneumoniae are Gram-negative facultative anaerobes that are found within host-associated commensal microbiomes, but they can also cause a wide range of infections that are often difficult to treat. These infections are caused by different pathotypes of K. pneumoniae, called either classical or hypervirulent strains. These two groups are genetically distinct, inhabit nonoverlapping geographies, and cause different types of harmful infections in humans. These distinct bacterial groups have also been found to interact differently with the host immune system. Initial innate immune defenses against K. pneumoniae infection include complement, macrophages, neutrophils, and monocytes; these defenses are primary strategies employed by the host to clear infections. K. pneumoniae pathogenesis depends upon the interactions between the microbe and each of these host defenses, and it is becoming increasingly apparent that bacterial genetic diversity impacts the outcomes of these interactions. Here, we highlight recent advances in our understanding of K. pneumoniae pathogenesis, with a focus on how bacterial evolution and diversity impact K. pneumoniae interactions with mammalian innate immune host defenses. We also discuss outstanding questions regarding how K. pneumoniae can frustrate normal immune responses, capitalize upon states of immunocompromise, and cause infections with high mortality.