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小鼠和人类动脉粥样硬化及心肌梗死中cathelicidin抗菌肽水平

Cathelicidin Antimicrobial Peptide Levels in Atherosclerosis and Myocardial Infarction in Mice and Human.

作者信息

Höpfinger Alexandra, Schmid Andreas, Karrasch Thomas, Pankuweit Sabine, Schäffler Andreas, Grote Karsten

机构信息

Department of Internal Medicine III, University of Giessen, Klinikstr. 33, 35392 Giessen, Germany.

Department of Cardiology and Angiology, Philipps-University Marburg, Baldinger Str., 35043 Marburg, Germany.

出版信息

Int J Mol Sci. 2024 Mar 2;25(5):2909. doi: 10.3390/ijms25052909.

DOI:10.3390/ijms25052909
PMID:38474156
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10931542/
Abstract

Obesity represents a worldwide health challenge, and the condition is accompanied by elevated risk of cardiovascular diseases caused by metabolic dysfunction and proinflammatory adipokines. Among those, the immune-modulatory cathelicidin antimicrobial peptide (human: CAMP; murine: CRAMP) might contribute to the interaction of the innate immune system and metabolism in these settings. We investigated systemic CAMP/CRAMP levels in experimental murine models of atherosclerosis, myocardial infarction and cardiovascular patients. Atherosclerosis was induced in low-density lipoprotein receptor-deficient (Ldlr) mice by high-fat diet (HFD). C57BL/6J wild-type mice were subjected to myocardial infarction by permanent or transient left anterior descending (LAD)-ligation. gene expression in murine organs and tissues was investigated via real-time PCR. Blood samples of 234 adult individuals with or without coronary artery disease (CAD) were collected. Human and murine CAMP/CRAMP serum levels were quantified by ELISA. Atherosclerotic mice exhibited significantly increased CRAMP serum levels and induced gene expression in the spleen and liver, whereas experimental myocardial infarction substantially decreased CRAMP serum levels. Human CAMP serum quantities were not significantly affected by CAD while being correlated with leukocytes and pro-inflammatory cytokines. Our data show an influence of cathelicidin in experimental atherosclerosis, myocardial infarction, as well as in patients with CAD. Further studies are needed to elucidate the pathophysiological mechanism.

摘要

肥胖是一项全球性的健康挑战，这种状况伴随着由代谢功能障碍和促炎脂肪因子导致的心血管疾病风险升高。其中，免疫调节性抗菌肽（人：CAMP；小鼠：CRAMP）可能在这些情况下促成先天免疫系统与新陈代谢之间的相互作用。我们研究了动脉粥样硬化、心肌梗死实验小鼠模型以及心血管疾病患者体内CAMP/CRAMP的全身水平。通过高脂饮食（HFD）在低密度脂蛋白受体缺陷（Ldlr）小鼠中诱导动脉粥样硬化。通过永久性或短暂性结扎左前降支（LAD）使C57BL/6J野生型小鼠发生心肌梗死。通过实时PCR研究小鼠器官和组织中的基因表达。收集了234名有或没有冠状动脉疾病（CAD）的成年个体的血样。通过ELISA对人和小鼠的CAMP/CRAMP血清水平进行定量。动脉粥样硬化小鼠的CRAMP血清水平显著升高，并且脾脏和肝脏中的基因表达增强，而实验性心肌梗死则使CRAMP血清水平大幅降低。人类CAMP血清量不受CAD的显著影响，但与白细胞和促炎细胞因子相关。我们的数据表明抗菌肽在实验性动脉粥样硬化、心肌梗死以及CAD患者中具有影响。需要进一步研究以阐明其病理生理机制。

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Circulating Concentrations of Cathelicidin Anti-Microbial Peptide (CAMP) Are Increased during Oral Glucose Tolerance Test.循环中抗菌肽（CAMP）的浓度在口服葡萄糖耐量试验期间增加。
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