Health disparities in COVID-19: immune and vascular changes are linked to disease severity and persist in a high-risk population in Riverside County, California.
Health disparities in COVID-19: immune and vascular changes are linked to disease severity and persist in a high-risk population in Riverside County, California.
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DOI：
10.1186/s12889-023-16462-5
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发表时间：
2023-08-19
影响因子：
4.5
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中科院分区：
文献类型：
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服务不足社区的健康差距，如医疗服务不足，影响COVID-19疾病的结果。这些差异在全国西班牙裔人口中很明显，感染率和死亡率不成比例地高。此外，受感染者可发展为长期COVID，对生活质量产生持续影响。本研究的目的是确定与滨江县（一个高风险且以西班牙裔为主的社区）的COVID-19结果相关的免疫和内皮因素，并调查COVID-19感染的长期影响。根据以下标准招募了加州州滨江县的112名参与者：健康对照组（n = 23），中度感染的门诊患者（门诊患者，n = 33），重度感染的ICU患者（住院患者，n = 33）和中度感染恢复的个体（n = 23）。对西班牙裔和非西班牙裔个体之间的结局差异以及合并症的存在/不存在进行了评价。通过ELISA、多重分析物测定和流式细胞术测量循环免疫和血管生物标志物。恢复后（n = 23）对长期COVID、肺部健康以及免疫和血管变化进行了随访评估，包括对相同参与者进行配对分析。与未感染的对照组相比，重度感染组的西班牙裔个体比例（n = 23，p = 0.012）高于中度感染组（n = 8，p = 0.550）。疾病严重程度与先天性单核细胞和中性粒细胞的变化、淋巴细胞减少症、细胞因子产生中断（IL-8和IP-10/CXCL 10增加，但IFNλ2/3和IFNγ减少）和内皮损伤增加（肌红蛋白，VCAM-1）相关。在严重感染组中，机器学习模型将LCN 2/NGAL，IL-6和单核细胞活化确定为与死亡相关的参数，而抗凝治疗与生存相关。从中度COVID感染中恢复导致长期免疫变化，包括单核细胞/淋巴细胞增加以及中性粒细胞和内皮标志物减少。该组的合并症比例较低（n = 8，p = 1.0），但尽管肺功能恢复，但仍报告了与长期COVID相关的症状。这项研究表明，在加州滨江县的西班牙裔个体中，COVID-19感染的严重程度增加。感染导致免疫和血管变化以及持续长达11个月的长期COVID症状，但肺容量和气流阻力恢复。鉴于长期COVID的免疫和行为影响，高风险人群感染易感性增加和生活质量下降的可能性值得进一步研究。在线版本包含补充材料，可通过10.1186/s12889-023-16462-5获得。
Health disparities in underserved communities, such as inadequate healthcare access, impact COVID-19 disease outcomes. These disparities are evident in Hispanic populations nationwide, with disproportionately high infection and mortality rates. Furthermore, infected individuals can develop long COVID with sustained impacts on quality of life. The goal of this study was to identify immune and endothelial factors that are associated with COVID-19 outcomes in Riverside County, a high-risk and predominantly Hispanic community, and investigate the long-term impacts of COVID-19 infection. 112 participants in Riverside County, California, were recruited according to the following criteria: healthy control (n = 23), outpatients with moderate infection (outpatient, n = 33), ICU patients with severe infection (hospitalized, n = 33), and individuals recovered from moderate infection (n = 23). Differences in outcomes between Hispanic and non-Hispanic individuals and presence/absence of co-morbidities were evaluated. Circulating immune and vascular biomarkers were measured by ELISA, multiplex analyte assays, and flow cytometry. Follow-up assessments for long COVID, lung health, and immune and vascular changes were conducted after recovery (n = 23) including paired analyses of the same participants. Compared to uninfected controls, the severe infection group had a higher proportion of Hispanic individuals (n = 23, p = 0.012) than moderate infection (n = 8, p = 0.550). Disease severity was associated with changes in innate monocytes and neutrophils, lymphopenia, disrupted cytokine production (increased IL-8 and IP-10/CXCL10 but reduced IFNλ2/3 and IFNγ), and increased endothelial injury (myoglobin, VCAM-1). In the severe infection group, a machine learning model identified LCN2/NGAL, IL-6, and monocyte activation as parameters associated with fatality while anti-coagulant therapy was associated with survival. Recovery from moderate COVID infection resulted in long-term immune changes including increased monocytes/lymphocytes and decreased neutrophils and endothelial markers. This group had a lower proportion of co-morbidities (n = 8, p = 1.0) but still reported symptoms associated with long COVID despite recovered pulmonary function. This study indicates increased severity of COVID-19 infection in Hispanic individuals of Riverside County, California. Infection resulted in immunological and vascular changes and long COVID symptoms that were sustained for up to 11 months, however, lung volume and airflow resistance was recovered. Given the immune and behavioral impacts of long COVID, the potential for increased susceptibility to infections and decreased quality of life in high-risk populations warrants further investigation. The online version contains supplementary material available at 10.1186/s12889-023-16462-5.
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影响因子：
4.5
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影响因子：
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作者：
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DOI：
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发表时间：
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期刊：
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影响因子：
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影响因子：
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