The emergence of the novel coronavirus in December 2019 in China marked the beginning of a pandemic that impacted healthcare systems and economic life all over the world. The virus primarily targets the respiratory system causing severe acute respiratory syndrome (SARS) in some patients, and therefore received the name of SARS-CoV-2. The pathogen stands out among other coronaviruses by its rapid transmission from human to human, with the majority of infected individuals being asymptomatic or presenting with only minor illness, therefore facilitating the pathogen spread. At the same time, people from the risk groups, such as the elderly, patients suffering from chronic diseases, or obese individuals, have increased chances of developing a severe or even fatal disease. The search for risk factors explaining this phenomenon continues. In this review, we focus on the known mechanisms of SARS-CoV-2 infection affecting the functioning of the immune system and discuss potential risk factors responsible for the severe disease course. Oxidative stress is one of such factors, which plays a prominent role in innate immunity activity, and recent research has revealed its tight involvement in SARS-CoV-2 infection. We discuss these recent findings and the development of excessive inflammation and cytokine storm observed during SARS-CoV-2 infection. Finally, we consider potential use of antioxidant drugs for alleviating the severe symptoms in affected patients.

The first references to neurotrophic factors date back to the middle of the 20th century when the nerve growth factor (NGF) was first discovered. Later studies delivered a large amount of data on neurotrophic factors. However, many questions regarding neurotrophin signaling still remain unanswered. One of the principal topics in neurotrophin research is their role in the immune system regulation. Another important research question is the possible involvement of neurotrophin signaling in the pathological processes associated with alcoholism. Among known neurotrophins, NT-4 remains the least studied and appears to be involved in alcoholism and chronic stress pathogenesis. In this review we discuss known neurotrophin signaling cascades mediated by different neurotrophin receptors, as well as provide a generalization of the data regarding the influence of neurotrophins NGF, BDNF, and NT-4 on the immune system and their potential contribution to the pathogenesis of alcoholism.

The aim was to evaluate the relationship between gut dysbiosis and hemodynamic changes (hyperdynamic circulation) in cirrhosis, and between hemodynamic changes and complications of this disease. This study included 47 patients with cirrhosis. Stool microbiome was assessed using 16S rRNA gene sequencing. Echocardiography with a simultaneous assessment of blood pressure and heart rate was performed to assess systemic hemodynamics. Patients with hyperdynamic circulation had more severe cirrhosis, lower albumin, sodium and prothrombin levels, higher C-reactive protein, aspartate aminotransferase and total bilirubin levels, and higher incidences of portopulmonary hypertension, ascites, overt hepatic encephalopathy, hypoalbuminemia, hypoprothrombinemia, systemic inflammation, and severe hyperbilirubinemia than patients with normodynamic circulation. Patients with hyperdynamic circulation compared with those with normodynamic circulation had increased abundance of Proteobacteria, Enterobacteriaceae, Bacilli, Streptococcaceae, Lactobacillaceae, Fusobacteria, Micrococcaceae, Intestinobacter, Clostridium sensu stricto, Proteus and Rumicoccus, and decreased abundance of Bacteroidetes, Bacteroidaceae, Holdemanella, and Butyrivibrio. The systemic vascular resistance and cardiac output values correlated with the abundance of Proteobacteria, Enterobacteriaceae, Bacilli, Streptococcaceae, Lactobacillaceae, Micrococcaceae, and Fusobacteria. Heart rate and cardiac output value were negatively correlated with the abundance of Bacteroidetes. The mean pulmonary artery pressure value was positively correlated with the abundance of Proteobacteria and Micrococcaceae, and negatively with the abundance of Holdemanella.

Background: Molecular immunoglobulin E ( IgE ) reactivity profiling with multiple micro‐arrayed allergens is a valuable tool in allergy diagnosis and has provided fundamental insights into the evolution of allergic sensitization in longitudinal birth cohort studies. However, there is a need for systematic cross‐sectional population‐based studies. Methods: A prospective, systematic and cross‐sectional population study was performed involving 1000 adult subjects from five centers (İstanbul, Ankara, İzmir, Kayseri, Samsun) representing different climatic areas of Türkiye (Turkey). In each center adult subjects with ( n = 100) and without ( n = 100) allergic symptoms who were born and grew up in the region were recruited. Subjects underwent skin prick testing with a panel of common aeroallergen extracts and were tested for IgE reactivity to 108 micro‐arrayed allergen molecules. Results: IgE reactivity profiles of respiratory allergens differed in the five centers according to the regional allergen exposome and climate. Interestingly, Kayseri with a high‐altitude, continental climate was identified as hypoallergenic region with low frequency of allergic symptoms and strongly reduced molecular sensitization rates. Between 31%–55% of subjects without allergic symptoms showed IgE sensitization to at least one of the allergens tested but allergen‐specific IgE levels, numbers of recognized allergens and rates of poly‐sensitization were more frequent in symptomatic individuals. Conclusions: This is the first comprehensive, systematic, prospective and cross‐sectional study investigating molecular IgE sensitization profiles in a region at the crossroads of Europe, Asia, and Africa with different climatic conditions. It reveals clinically relevant differences in regional molecular IgE sensitization profiles depending on the allergen exposome and identifies a hypoallergenic region with distinct climatic features.

We aimed to systematize the results of published studies on the use of Saccharomyces boulardii (SB) for the treatment of various liver disorders (CRD42022378050). Searches were conducted using PubMed and Scopus on 1 August 2022. The PubMed search was updated on 15 June 2024. The review included sixteen studies: ten experimental animal studies (EASs) and six randomized controlled trials (RCTs). The CNCM I-745 strain was used in 68.8% of the included studies. SB reduced the severity of many manifestations of cirrhosis, and lowered the Child–Pugh scores in RCT. SB reduced the serum concentrations of TNF-α, IL-1β, IL-6, and IL-4 in animals with metabolic dysfunction-associated steatotic liver disease (MASLD); lowered the serum TNF-α and IL-6 levels in experimental cirrhosis in rats; and reduced the CRP levels in decompensated cirrhosis. The EAS of MASLD revealed that SB reduced liver steatosis and inflammation and lowered the liver expression of genes of TNF-α, IL-1β, interferon-γ, and IL-10. In studies on experimental cirrhosis and MASLD, SB reduced the liver expression of genes of TGF-β, α-SMA, and collagen as well as liver fibrosis. SB reduced the abundance of Escherichia (Proteobacteria), increased the abundance of Bacteroidetes in the gut microbiota, prevented an increase in intestinal barrier permeability, and reduced bacterial translocation and endotoxemia.

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