Abstract
Pathogenetic progression mechanisms in the SARS-CoV-2–essential hypertension (EAH) system are more complex than interaction at the level of angiotensinconverting enzyme 2 (ACE2). The study was aimed to assess the dynamic changes of the IL1 members (IL1β, IL1α, IL1ra, IL18, IL18BP, IL37) blood levels in patients with EAH 10, 30, and 180 days after having COVID-19 in order to define cytokine-mediated mechanisms of EAH progression during the period following infection. The study involved four groups of patients: with a history of EAH and COVID-19 (pneumonia/no pneumonia), with a history of COVID-19 (pneumonia/no pneumonia) and no EAH. Cytokine levels were determined by enzyme immunoassay. The study results demonstrate the prolonged proinflammatory immune response during the period following infection in patients with EAH (retaining higher levels of IL1β, IL1α, and IL18 on days 10, 30, and 180 after recovery (р < 0.001) compared to levels measured prior to SARS-CoV-2 infection). In the group with no EAH, the balance of assayed cytokines was restored on day 30 of follow-up. The two-fold increase of blood IL18 levels in patients, having a history of EAH and COVID-19 and showing no increase in the IL18ВР levels after 30 days of follow up compared to the values measured prior to infection, is associated with cardiovascular complications occurring during the first six months of follow-up. This makes it possible to hypothesize the importance of these immunoregulatory peptides for the pathogenesis of complications and enhances the relevance of further scientific research.
Highlights
Compliance with ethical standards: the study was approved by the Ethics Committee of the National Research Mordovia State University, the research was carried out in accordance with the WMA Declaration of Helsinki (2013) and the protocol of the Convention on Human Rights and Biomedicine (1999) taking into consideration the Additional Protocol to the Convention on Human Rights and Biomedicine, concerning Biomedical Research (2005)
Prior to SARS-CoV-2 infection, the patients with stage 2 essential hypertension (EAH) were characterized by higher IL1β, IL1α, IL18, IL18BP, and IL37 levels in peripheral blood serum compared to generally healthy individuals (р < 0.001) (Tables 1 and 2)
After having COVID-19, the different quantitative and qualitative indicators, reflecting dynamic changes of blood IL1β, IL1α, IL1ra, IL18, IL18BP, and IL37 levels, were measured in patients with stage 2 EAH compared to patients who had been infected with SARSCoV-2 but had no EAH
Summary
Compliance with ethical standards: the study was approved by the Ethics Committee of the National Research Mordovia State University (protocol No 12 dated December 14, 2008, protocol No 85 dated May 27, 2020), the research was carried out in accordance with the WMA Declaration of Helsinki (2013) and the protocol of the Convention on Human Rights and Biomedicine (1999) taking into consideration the Additional Protocol to the Convention on Human Rights and Biomedicine, concerning Biomedical Research (2005). Целью исследования было проанализировать динамику содержания представителей семейства IL1 (IL1β, IL1α, IL1ra, IL18, IL18BP, IL37) в крови больных ЭАГ через 10, 30 и 180 дней после COVID-19 для определения цитокинопосредованных звеньев прогрессирования ЭАГ в постинфекционном периоде. Полученные результаты демонстрируют пролонгированный характер провоспалительного иммунного ответа в постинфекционном периоде у больных с ЭАГ (сохранение более высоких уровней IL1β, IL1α, IL18 на 10-й, 30-й и 180-й дни после выздоровления (р < 0,001) при сопоставлении с периодом до инфицирования SARS-CoV-2). It is important to consider the delayed effects of SARS-CoV-2 realized through imbalance of cytokine-mediated vectors, underlying the progression of a number of cardiovascular disorders during the period following infection, and the increased risk of complications [2, 3]. In addition to the conclusion that individuals with AH may be more susceptible to COVID-19 and are characterized by more severe course of the disease [7, 8], the literature reports that the SARS-CoV-2 infection may trigger both the progression of pre-existing pathological process, and the initiation of different pathological process [3]
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