Coronavirus disease 2019 (COVID-19) has swept the world, unlike any other pandemic in the last 50 years. Our understanding of the disease has evolved rapidly since the outbreak; disease prognosis is influenced mainly by multi-organ involvement. Acute respiratory distress syndrome, heart failure, renal failure, liver damage, shock and multi-organ failure are strongly associated with morbidity and mortality. The COVID-19 disease pathology is plausibly linked to the hyperinflammatory response of the body characterized by pathological cytokine levels. The term ‘cytokine storm syndrome’ is perhaps one of the critical hallmarks of COVID-19 disease severity. In this review, we highlight prominent cytokine families and their potential role in COVID-19, the type I and II interferons, tumour necrosis factor and members of the Interleukin family. We address various changes in cellular components of the immune response corroborating with changes in cytokine levels while discussing cytokine sources and biological functions. Finally, we discuss in brief potential therapies attempting to modulate the cytokine storm.

Global deployment of an effective and safe vaccine is necessary to curtail the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here, we evaluated a Newcastle disease virus (NDV)-based vectored-vaccine in mice and hamsters for its immunogenicity, safety and protective efficacy against SARS-CoV-2. Intranasal administration of recombinant (r)NDV-S vaccine expressing spike (S) protein of SARS-CoV-2 to mice induced high levels of SARS-CoV-2-specific neutralizing immunoglobulin A (IgA) and IgG2a antibodies and T cell-mediated immunity. Hamsters immunised with two doses of vaccine showed complete protection from lung infection, inflammation, and pathological lesions following SARS-CoV-2 challenge. Importantly, administration of two doses of intranasal rNDV-S vaccine significantly reduced the SARS-CoV-2 shedding in nasal turbinate and lungs in hamsters. Collectively, intranasal vaccination has the potential to control infection at the site of inoculation, which should prevent both clinical disease and virus transmission to halt the spread of the COVID-19 pandemic.

Autism spectrum disorders (ASD) consist of a range of neurodevelopmental conditions accompanied by dysbiosis of gut microbiota. Therefore, a number of microbiota manipulation strategies were developed to restore their balance. However, a comprehensive comparison of the various methods on gut microbiota is still lacking. Here, we evaluated the effect of Bifidobacterium (BF) treatment and fecal microbiota transplantation (FT) on gut microbiota in a propionic acid (PPA) rat model of autism using 16S rRNA sequencing. Following PPA treatment, gut microbiota showed depletion of Bacteroidia and Akkermansia accompanied by a concomitant increase of Streptococcus, Lachnospiraceae, and Paraeggerthella. The dysbiosis was predicted to cause increased levels of porphyrin metabolism and impairments of acyl-CoA thioesterase and ubiquinone biosynthesis. On the contrary, BF and FT treatments resulted in a distinct increase of Clostridium, Bifidobacterium, Marvinbryantia, Butyricicoccus, and Dorea. The taxa in BF group positively correlated with vitamin B12 and flagella biosynthesis, while FT mainly enriched flagella biosynthesis. In contrast, BF and FT treatments negatively correlated with succinate biosynthesis, pyruvate metabolism, nitrogen metabolism, beta-Lactam resistance, and peptidoglycan biosynthesis. Therefore, the present study demonstrated that BF and FT treatments restored the PPA-induced dysbiosis in a treatment-specific manner.

The new wave of anti-migraine agents is nothing less than a milestone in our battle to manage this devastating disease. However, concerns have recently increased regarding the safety of these drugs. CGRP, while known as a potent vasodilator, is also a key neural and immune modulator. The roles of CGRP in immune determination, have been studied in depth, with particular focus on its functional significance with respect to common immune challenges i.e., bacterial, viral, fungal and parasitic infections. This review discusses many potential areas of concern in regard to blocking CGRP function and its potential influence on immune milieus during infection, and the risk of adverse effects. Finally, this review recommends specific measures to be taken into consideration when administering anti-CGRP/CGRPR agents.

This study aimed to investigate the relationship between gastrointestinal tract infection and dengue hemorrhagic fever. Dengue hemorrhagic fever is a syndrome caused by the dengue virus and primarily affects children below ten years of age and is spread by the Aedes aegypti mosquito. Gastrointestinal tract infection is a bacterial and parasitic infection that leads to gastrointestinal tract inflammation which involves the small intestine and the stomach. The relationship between the two can be manifested by gastrointestinal bleeding, acute pancreatitis, and fulminant liver failure. In this research work, 600 blood and feces samples of different ages and sex (7-8 worms) were collected from Jeddah city. From the blood samples, serum was made and stored at -20°C until use. The frozen sera samples were investigated for sero-detection of DENV-NS1 antigen as a rapid, sensitive, and cost-effective test to detect asymptomatic acute DENV-infected donors and anti-DENV IgM and IgG antibodies. Feces samples were processed for the detection of parasites. The data acquired from these samples of all the 600 participants were analyzed and interpreted, followed by statistical analysis using GraphPad Prism 5.0 software. All the values were considered significant, which showed a value of less than 0.05. Results were expressed as with the range. This article documents that gastrointestinal tract manifestations frequently occur among patients with dengue hemorrhagic fever. There are close relationships between gastrointestinal tract infection and dengue hemorrhagic fever. In current work, it was established that dengue fever leads to gastrointestinal tract bleeding in the presence of intestinal parasites. Therefore, failure to identify the patients with this infection early enough can lead to an increased morbidity and mortality rate.

Background: Epidermal growth factor (EGF) plays a crucial role in cellular growth, differentiation, and pancreatic β-cell maintenance. Despite reports on EGF deficiency in diabetic animal models, its relevance in type 2 diabetes (T2D), particularly in relation to obesity, remains underexplored. The present study aimed to evaluate plasma EGF levels in individuals with and without T2D, assess its associations with glycaemic status and clinical parameters, and evaluate the influence of obesity on these relationships. Methods: A total of 838 eligible participants were selected from the Kuwait Diabetes Epidemiology Program. Of those, 428 were included in a 1:1 case–control analysis (214 T2D and 214 non-diabetics). EGF was measured in plasma using ELISA. Associations between EGF with glycaemic and clinical variables were evaluated using Pearson’s correlation, multiple linear regression, and logistic regression analyses. Results: Plasma EGF levels were significantly lower in individuals with T2D compared to non-diabetics (P < 0.001). Among non-diabetics, obese participants had a significantly lower EGF level than their non-obese counterparts (P = 0.03), while no such difference was observed in T2D. EGF negatively correlated with fasting blood glucose in both non-diabetics (P = 0.004) and T2D individuals (P < 0.001). In T2D, EGF negatively correlated with haemoglobin A1C (HbA1C) (P = 0.001), triglyceride (TG) (P = 0.021), and waist-to-hip ratio (WHR) (P = 0.014). Logistic regression confirmed that lower EGF levels were independently associated with T2D but not with general obesity (OR = 0.996, P = 0.001). Conclusion: Reduced EGF levels are associated with poor glycaemic control in T2D. These findings highlight EGF’s potential as a biomarker for glycaemic dysregulation and support further investigation into its role in diabetes pathophysiology and complications.