The impact of prior SARS-CoV-2 infection on host inflammatory cytokine profiles in patients with TB or other respiratory diseases.
The impact of prior SARS-CoV-2 infection on host inflammatory cytokine profiles in patients with TB or other respiratory diseases.
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DOI：
10.3389/fimmu.2023.1292486
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发表时间：
2023
影响因子：
7.3
通讯作者：
中科院分区：
文献类型：
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作者：
结核病和COVID-19是全球传染病死亡的两个主要原因，它们的重叠可能是频繁和不可避免的。先前的研究表明，结核病/ COVID-19合并感染者的死亡率增加，新出现的证据表明，COVID-19可能增加对结核病的易感性。然而，这些相互作用的免疫学机制尚不清楚。在这项研究中，我们旨在阐明先前或同时感染COVID-19对结核病患者和其他呼吸道疾病（ORD）患者免疫谱的影响。收集了161名冈比亚青少年和成人结核病或慢性阻塞性肺炎患者的血清和鼻咽样本，采用PCR方法确定同时感染COVID-19，并通过抗体血清阳性确定既往感染COVID-19。多重细胞因子免疫测定法用于在基线和结核病患者治疗过程中定量患者血清样本中的27种细胞因子和趋化因子。引人注目的是，与未感染COVID-19的TB和ORD患者相比，发现先前感染的TB和ORD患者的几种细胞因子表达显著降低，包括IL-1β， TNF-α和IL-7 （p<0.035）。在抗结核治疗6个月时，血清阳性患者血清碱性FGF （p=0.0115）、IL-1β (p=0.0326)和IL-8 （p=0.0021）均低于血清阴性患者。结核合并急性COVID-19患者IL-8、IL-13、TNF-α和IP-10水平低于单纯结核患者，但差异无统计学意义（p < 0.05）。我们的研究结果表明，COVID-19感染改变了随后对TB和ORDs的反应，可能有助于发病机制。需要进一步的工作来确定COVID-19感染是否会加速结核病的进展，尽管我们的结果在实验上支持这一假设。
Tuberculosis (TB) and COVID-19 are the two leading causes of infectious disease mortality worldwide, and their overlap is likely frequent and inevitable. Previous research has shown increased mortality in TB/COVID-coinfected individuals, and emerging evidence suggests that COVID-19 may increase susceptibility to TB. However, the immunological mechanisms underlying these interactions remain unclear. In this study, we aimed to elucidate the impact of prior or concurrent COVID-19 infection on immune profiles of TB patients and those with other respiratory diseases (ORD). Serum and nasopharyngeal samples were collected from 161 Gambian adolescents and adults with either TB or an ORD. Concurrent COVID-19 infection was determined by PCR, while prior COVID-19 was defined by antibody seropositivity. Multiplex cytokine immunoassays were used to quantify 27 cytokines and chemokines in patient serum samples at baseline, and throughout treatment in TB patients. Strikingly, TB and ORD patients with prior COVID-19 infection were found to have significantly reduced expression of several cytokines, including IL-1β, TNF-α and IL-7, compared to those without (p<0.035). Moreover, at month-six of anti-TB treatment, seropositive patients had lower serum Basic FGF (p=0.0115), IL-1β (p=0.0326) and IL-8 (p=0.0021) than seronegative. TB patients with acute COVID-19 coinfection had lower levels of IL-8, IL-13, TNF-α and IP-10 than TB-only patients, though these trends did not reach significance (p>0.035). Our findings demonstrate that COVID-19 infection alters the subsequent response to TB and ORDs, potentially contributing to pathogenesis. Further work is necessary to determine whether COVID-19 infection accelerates TB disease progression, though our results experimentally support this hypothesis.
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影响因子：
5.6
作者：
Pelaia C;Heffler E;Crimi C;Maglio A;Vatrella A;Pelaia G;Canonica GW
通讯作者：
Canonica GW
影响因子：
2.7
作者：
Liu QY;Han F;Pan LP;Jia HY;Li Q;Zhang ZD
通讯作者：
Zhang ZD
影响因子：
15.1
作者：
Cilloni L;Fu H;Vesga JF;Dowdy D;Pretorius C;Ahmedov S;Nair SA;Mosneaga A;Masini E;Sahu S;Arinaminpathy N
通讯作者：
Arinaminpathy N
影响因子：
64.8
作者：
通讯作者：
--
影响因子：
15.9
作者：
Riou, Catherine;du Bruyn, Elsa;Wilkinson, Robert J.
通讯作者：
Wilkinson, Robert J.