Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was originated in November–December 2019 in Wuhan, China, and has rapidly spread around the world causing severe health and socioeconomical damage to the entire civilization. The key feature of coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, is upper respiratory tract infection, which may be complicated by bilateral pneumonia. Angiotensin converting enzyme 2 (ACE2) has been identified as a key host factor, required for virus entry into cells. Interestingly, ACE2 is expressed not only in the respiratory system, but also in the other organs and systems including adrenal glands. Here we provide the first description of the pathomorphological changes in adrenal glands in patients with severe COVID-19 characterized by perivascular infiltration of CD3+ and CD8+ T-lymphocytes. Due to the central role of the adrenals in the stress response of the organism, this finding is of potential clinical relevance, because infection with the SARS-CoV-2 virus might critically impair adrenal function under pathophysiological conditions.

Background: Arterial hypertension (AH) is associated with heart and chronic kidney disease (CKD). However, the precise mechanisms of myocardial remodeling (MR) in the settings of CKD remain elusive. We hypothesized that TRPC6, calcineurin/NFAT, and Wnt/β-catenin signaling pathways are involved in the development of MR in the background of CKD and AH. Methods: Early CKD was induced by performing a 5/6 nephrectomy (5/6NE) in spontaneously hypertensive rats (SHR-NE). Sham-operated (SO) SHR (SHR-SO) and Wistar Kyoto (WKY-SO) rats served as controls. Systolic blood pressure (SBP), heart rate, myocardial mass index (MMI), serum creatinine, cardiomyocyte diameter (dCM), myocardial fibrosis (MF), serum and kidney α-Klotho levels, myocardial expression of calcineurin (CaN), TRPC6, and β-catenin were measured two months after 5/6NE or SO. Results: NE-induced kidney dysfunction corresponded to mild-to-moderate human CKD and was associated with an increase in FGF23 and a decrease in renal α-Klotho. The levels of SBP, MMI, dCM, and MF were higher in SHRs compared to WKY-SO as well as in SHR-NE vs. SHR-SO. The MR was associated with increased cardiomyocyte expression of CaN/NFAT and β-catenin along with its intracellular re-distribution. TRPC6 protein levels were substantially elevated in both SHR groups with higher Trpc6 mRNA expression in SHR-NE. Conclusions: The Wnt/β-catenin and TRPC6/CaN/NFAT hypertrophic signaling pathways seem to be involved in myocardial remodeling in the settings of AH and CKD and might be mediated by FGF23 and α-Klotho axis.

Новая коронавирусная инфекция (COVID-19) представляет собой глобальную проблему человечества. Среди её важнейших аспектов, требующих углублённого изучения, – патогенез и морфологические изменения при тяжелых формах заболевания. Материалы и методы. Проведен анализ 18 летально закончившихся случаев. Наряду с рутинной оценкой макро- и микроскопических изменений, проведено иммуногистохимическое исследование легких и других органов с использованием сывороток к СD 2, 3, 4, 5, 7, 20, 31, 34, 56, 57, 69, также в легких и печени выявлялось наличие Fe2+ и Fe3+. Результаты. Показаны характерные структурные изменения легких, которые могут быть связаны с цитопатическим и цитопролиферативным действием вируса с поражением как мерцательного, так и альвеолярного эпителия, а также формированием гиалиновых мембран. Клеточная инфильтрация представлена преимущественно супрессорными популяциями Т-лимфоцитов и макрофагами. Выявлены повреждения эндотелия, тромбоз сосудов разного калибра и кровоизлияния. Во многих органах (лимфатических узлах, селезенке, кишечнике, головном мозге, надпочечниках) обнаружены изменения, возможно, свидетельствующие о генерализации вирусной инфекции, а инфильтрация CD8+ лимфоцитами в почках, печени, надпочечниках, перикарде, кишечнике свидетельствует о вероятном аутоиммунном компоненте патогенеза. В печени и легких умерших от COVID-19 не выявлено значимого скопления гранул Fe3+и Fe2+.

In this study, we investigated the effect of three different probiotics, namely, a combination of Lactobacillus acidophilus (LA–5) and Bifidobacterium animalis subsp. lactis (BB–12), Saccharomyces boulardii, and Enterococcus faecium L3 on myocardial infarct size in rats with diet-induced obesity (DIO) and chemically-induced colitis (CIC). Potential associations between the effects of probiotics on myocardial ischemia-reperfusion injury and gut microbiome patterns as well as the serum levels of pro- and anti-inflammatory cytokines, lipopolysaccharide, and short chain fatty acids were also studied. Intragastric administration of lyophilized Lactobacillus acidophilus and Bifidobacterium animalis subsp. lactis at a dose of 1.2 × 10⁸ CFU/mL for 15 days resulted in myocardial infarct size reduction in rats with DIO, CIC, and antibiotic-induced dysbiosis. This cardioprotective effect was associated with specific changes in cytokine concentrations, namely reduced levels of IL–1β, TNF–α, IL–2, and IL–8. At the same time, the use of Lactobacillus acidophilus and Bifidobacterium animalis subsp. lactis was accompanied by a significant reduction in lipopolysaccharide level, suggesting normalization of intestinal epithelial barrier permeability. However, the cardioprotective effect of Lactobacillus acidophilus and Bifidobacterium animalis subsp. lactis is not secondary to improved healing of the intestinal mucosa in CIC, as evidenced by the lack of difference in histopathological scores.

The development of biocompatible composite materials is in high demand in many fields such as biomedicine, bioengineering, and biotechnology. In this study, two series of poly (D,L-lactide) and poly (ε-caprolactone)-based films filled with neat and modified with poly (glutamic acid) (PGlu) nanocrystalline cellulose (NCC) were prepared. An analysis of scanning electron and atomic force microscopies’ results shows that the modification of NCC with poly (glutamic acid) favored the better distribution of the nanofiller in the polymer matrix. Investigating the ability of the developed materials to attract and retain calcium ions led to the conclusion that composites containing NCC modified with PGlu induced better mineralization from model solutions than composites containing neat NCC. Moreover, compared to unmodified NCC, functionalization with PGlu improved the mechanical properties of composite films. The subcutaneous implantation of these composite materials into the backs of rats and the further histological investigation of neighboring tissues revealed the better biocompatibility of polyester materials filled with NCC–PGlu.