Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its associated symptoms, named coronavirus disease 2019 (COVID-19), have rapidly spread worldwide, resulting in the declaration of a pandemic. When several countries began enacting quarantine and lockdown policies, the pandemic as it is now known truly began. While most patients have minimal symptoms, approximately 20% of verified subjects are suffering from serious medical consequences. Co-existing diseases, such as cardiovascular disease, cancer, diabetes, and others, have been shown to make patients more vulnerable to severe outcomes from COVID-19 by modulating host-viral interactions and immune responses, causing severe infection and mortality. In this review, we outline the putative signaling pathways at the interface of COVID-19 and several diseases, emphasizing the clinical and molecular implications of concurring diseases in COVID-19 clinical outcomes. As evidence is limited on co-existing diseases and COVID-19, most findings are preliminary, and further research is required for optimal management of patients with comorbidities.

• Klíčová slova
• COVID-19, cancer, cardiovascular disease, coronavirus disease 2019, diabetes, immune responses, treatment implications,
• MeSH
• COVID-19 * epidemiologie   MeSH
• karanténa MeSH
• kontrola infekčních nemocí MeSH
• lidé MeSH
• pandemie MeSH
• SARS-CoV-2 MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

BACKGROUND/OBJECTIVES: Hyperglycemia represents one of possible mediators for activation of immune system and may contribute to worsening of inflammatory state associated with obesity. The aim of our study was to investigate the effect of a short-term hyperglycemia (HG) on the phenotype and relative content of immune cells in circulation and subcutaneous abdominal adipose tissue (SAAT) in obese women without metabolic complications. SUBJECTS/METHODS: Three hour HG clamp with infusion of octreotide and control investigations with infusion of octreotide or saline were performed in three groups of obese women (Group1: HG, Group 2: Octreotide, Group 3: Saline, n=10 per group). Before and at the end of the interventions, samples of SAAT and blood were obtained. The relative content of immune cells in blood and SAAT was determined by flow cytometry. Gene expression analysis of immunity-related markers in SAAT was performed by quantitative real-time PCR. RESULTS: In blood, no changes in analysed immune cell population were observed in response to HG. In SAAT, HG induced an increase in the content of CD206 negative monocytes/macrophages (p<0.05) and T lymphocytes (both T helper and T cytotoxic lymphocytes, p<0.01). Further, HG promoted an increase of mRNA levels of immune response markers (CCL2, TLR4, TNFα) and lymphocyte markers (CD3g, CD4, CD8a, TBX21, GATA3, FoxP3) in SAAT (p<0.05 and 0.01). Under both control infusions, none of these changes were observed. CONCLUSIONS: Acute HG significantly increased the content of monocytes and lymphocytes in SAAT of healthy obese women. This result suggests that the short-term HG can modulate an immune status of AT in obese subjects.

• MeSH
• biologické markery metabolismus   MeSH
• C-peptid krev   MeSH
• dospělí MeSH
• fenotyp MeSH
• hyperglykemie krev   chemicky indukované   komplikace   imunologie   MeSH
• inzulin krev   MeSH
• krevní glukóza metabolismus   MeSH
• lidé MeSH
• makrofágy cytologie   účinky léků   MeSH
• messenger RNA genetika   metabolismus   MeSH
• monocyty cytologie   účinky léků   MeSH
• obezita komplikace   MeSH
• oktreotid farmakologie   MeSH
• počet buněk MeSH
• podkožní břišní tuk účinky léků   imunologie   MeSH
• regulace genové exprese účinky léků   MeSH
• T-lymfocyty cytologie   účinky léků   MeSH
• zdraví * MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• klinická studie MeSH
• práce podpořená grantem MeSH
• Názvy látek
• biologické markery MeSH
• C-peptid MeSH
• inzulin MeSH
• krevní glukóza MeSH
• messenger RNA MeSH
• oktreotid MeSH

AIMS: The aim of this study was to evaluate the effect of acute glycemia increase on microvasculature and endothelium in Type 1 diabetes during hyperinsulinemic clamp. PATIENTS AND METHODS: Sixteen patients (51 ± 7 yrs) without complications were examined during iso- and hyperglycemic clamp (glucose increase 5.5 mmol·L(-1)). Insulin, lipid parameters, cell adhesion molecules and fibrinogen were analyzed. Microvascular reactivity (MVR) was measured by laser Doppler flowmetry. RESULTS: Maximum perfusion and the velocity of perfusion increase during PORH were higher in hyperglycemia compared to baseline (47 ± 16 versus 40 ± 16 PU, P < 0.01, and 10.4 ± 16.5 versus 2.6 ± 1.5 PU·s(-1), P < 0.05, resp.). Time to the maximum perfusion during TH was shorter and velocity of perfusion increase during TH higher at hyperglycemia compared to isoglycemic phase (69 ± 15 versus 77 ± 16 s, P < 0.05, and 1.4 ± 0.8 versus 1.2 ± 0.7 PU·s(-1), P < 0.05, resp.). An inverse relationship was found between insulinemia and the time to maximum perfusion during PORH (r = -0.70, P = 0.007). CONCLUSION: Acute glycemia did not impair microvascular reactivity in this clamp study in Type 1 diabetic patients. Our results suggest that insulin may play a significant role in the regulation of microvascular perfusion in patients with Type 1 diabetes through its vasodilation effect and can counteract the effect of acute glucose fluctuations.

• MeSH
• cévní endotel cytologie   MeSH
• diabetes mellitus 1. typu patofyziologie   terapie   MeSH
• dospělí MeSH
• glykemický clamp * MeSH
• hyperglykemie patofyziologie   terapie   MeSH
• inzulin metabolismus   MeSH
• kalibrace MeSH
• komplikace diabetu patologie   MeSH
• krevní glukóza metabolismus   MeSH
• laser doppler flowmetrie metody   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mikrocirkulace MeSH
• oxidační stres MeSH
• perfuze MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• inzulin MeSH
• krevní glukóza MeSH