Interleukin-37: A Link Between COVID-19, Diabetes, and the Black Fungus.
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ABSTRACT:
SUBMITTER: Tokajian S
PROVIDER: S-EPMC8793130 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Early in the COVID-19 pandemic, type 2 diabetes (T2D) was marked as a risk-factor for severe disease. Inflammation is central to the aetiology of both conditions where immune responses influence disease course. Identifying at-risk groups through immuno-inflammatory signatures can direct personalised care and help develop potential targets for precision therapy. This observational study characterised immunophenotypic variation associated with COVID-19 severity in T2D. Broad-spectrum immunophenotyping quantified 15 leukocyte populations in circulation from a cohort of 45 hospitalised COVID-19 patients with and without T2D. Lymphocytopenia, of CD8+ lymphocytes, was associated with severe COVID-19 and intensive care admission in non-diabetic and T2D patients. A morphological anomaly of increased monocyte size and monocytopenia of classical monocytes were specifically associated with severe COVID-19 in patients with T2D requiring intensive care. Over-expression of inflammatory markers reminiscent of the type-1 interferon pathway underlaid the immunophenotype associated with T2D. These changes may contribute to severity of COVID-19 in T2D. These findings show characteristics of severe COVID-19 in T2D as well as provide evidence that type-1 interferons may be actionable targets for future studies.
| S-SCDT-EMM-2020-13038 | biostudies-other
Project description:In Diabetes Mellitus the loss of capacity to regulate immunity, the reduction of pulmonary functions and the pro-thrombotic state determine the severity of COVID-19.
| S-EPMC7260494 | biostudies-literature
Project description:Background Coronavirus disease 2019 (COVID-19) is a pandemic viral infection that has ravaged the world in recent times, and the associated morbidity and mortality have been much more pronounced in those with noncommunicable disease. Diabetes mellitus is one of commonest noncommunicable diseases associated with worsening clinical status in COVID-19 patients. Summary The aim of this review was to evaluate the receptors and pathogenetic link between diabetes and COVID-19. Both disease conditions involve inflammation with the release of inflammatory markers. The roles of angiotensin-converting enzyme molecule and dipeptidyl peptidase were explored to show their involvement in COVID-19 and diabetes. Pathogenetic mechanisms such as impaired immunity, microangiopathy, and glycemic variability may explain the effect of diabetes on recovery of COVID-19 patients. The effect of glucocorticoids and catecholamines, invasion of the pancreatic islet cells, drugs used in the treatment of COVID-19, and the lockdown policy may impact negatively on glycemic control of diabetic patients. The outcome studies between diabetic and nondiabetic patients with COVID-19 were also reviewed. Some drug trials are still ongoing to determine the suitability or otherwise of some drugs used in diabetic patients with COVID-19, such as dapagliflozin trial and linagliptin trial.
| S-EPMC7649685 | biostudies-literature
Project description:Several countries around the world have faced an important obesity challenge for the past four decades as the result of an obesogenic environment. This disease has a multifactorial origin and it is associated with multiple comorbidities including type 2 diabetes, hypertension, osteoarthritis, metabolic syndrome, cancer, and dyslipidemia. With regard to dyslipidemia, hypertriglyceridemia is a well-known activator of the NLRP3 inflammasome, triggering adipokines and cytokines secretion which in addition induce a systemic inflammatory state that provides an adequate scenario for infections, particularly those mediated by viruses such as HIV, H1N1 influenza, and SARS-CoV-2. The SARS-CoV-2 infection causes the coronavirus disease 2019 (COVID-19) and it is responsible for the pandemic that we are currently living. COVID-19 causes an aggressive immune response known as cytokine release syndrome or cytokine storm that causes multiorgan failure and in most cases leads to death. In the present work, we aimed to review the molecular mechanisms by which obesity-associated systemic inflammation could cause a more severe clinical presentation of COVID-19. The SARS-CoV-2 infection could potentiate or accelerate the pre-existing systemic inflammatory state of individuals with obesity, via the NLRP3 inflammasome activation and the release of pro-inflammatory cytokines from cells trough Gasdermin-pores commonly found in cell death by pyroptosis.
| S-EPMC7662564 | biostudies-literature
Project description:The deadly second wave of COVID-19 has seen an unprecedented surge in mucormycosis associated mortality in India, overwhelming the heath authorities with challenges beyond measure. Also known as black fungus, this life-threatening fungal infection usually manifests in the nose, spreads to the eyes, and in some cases also to the brain. Immune suppression, pre-existing conditions, prolonged and indiscriminate use of steroids, and unhygienic environments are some of the widely recognized risk factors for contracting black fungus in individuals recovered from COVID-19. However, diagnosis of the infection remains insufficient due to the lack a holistic understanding of the possible risks, symptoms, and exposure pathways and therefore no definite protocol exists for managing this fatal infection. Here, we synthesize the current state of knowledge on black fungus outbreak in India and identify key gaps in its understanding with respect to potential risk factors leading to the widespread infection. We looked at 3354 black fungus cases in India, enlisting ailment history (particularly diabetes) and steroid usage in COVID-19 patients as the key factors responsible for exacerbating risks associated with the disease. However, we also press on the possibilities that other less studied non-traditional risk factors may also have a role in causing the infection. Black fungus is therefore a reality of COVID-19, with or without diabetes or steroid use needs to be investigated. We believe such a review is imperative for making informed decisions specially around timely diagnosis and channelizing efforts in controlling the spread of COVID-19 associated mucormycosis.
| S-EPMC8816797 | biostudies-literature
Project description:Although some studies reported the comprehensive mRNA expression analysis of coronavirus disease 2019 (COVID-19) using blood samples to understand its pathogenesis, the characteristics of RNA expression in COVID-19 and sepsis have not been compared. We compared the transcriptome expression of whole blood samples from patients with COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and patients with sepsis caused by other bacteria who entered the intensive care unit to clarify the COVID-19-specific RNA expression and understand its pathogenesis. Transcriptomes related to mitochondria were upregulated in COVID-19, whereas those related to neutrophils were upregulated in sepsis. However, the transcriptomes related to neutrophils were upregulated in both COVID-19 and sepsis compared to in healthy controls, whereas the mitochondrial transcriptomes were upregulated in COVID-19 and downregulated in sepsis compared to in healthy controls. Moreover, sepsis showed sub-optimal intrinsic apoptotic features compared with COVID-19. The transcriptome expression of COVID-19 has been examined in vitro but has not been widely validated using human specimens. This study improves the understanding of the pathogenesis of COVID-19 and can contribute to the development of treatments.
2022-11-29 | GSE199816 | GEO
Project description:BackgroundThere is very limited comprehensive information on disparate outcomes of black and white patients with COVID-19 infection. Reports from cities and states have suggested a discordant impact on black Americans, but no nationwide study has yet been performed. We sought to understand the differential outcomes for black and white Americans infected with COVID-19.MethodsWe obtained case-level data from the Centers for Disease Control and Prevention on 76,442 white and 48,338 non-Hispanic Black patients diagnosed with COVID-19, ages 0 to >80+, outlining information on hospitalization, ICU admission, ventilation, and death outcomes. Multivariate Poisson regressions were used to estimate the association of race, treating white as the reference group, controlling for sex, age group, and the presence of comorbidities.ResultsBlack patients were generally younger than white, were more often female, and had larger numbers of comorbidities. Compared to white patients with COVID-19, black patients had 1.4 times the risk of hospitalization (RR 1.42, p < 0.001), and almost twice the risk of requiring ICU care (RR 1.68, p < 0.001) or ventilatory support (RR 1.81, p < 0.001) after adjusting for covariates. Black patients saw a 1.36 times increased risk of death (RR 1.36, p < 0.001) compared to white. Disparities between black and white outcomes increased with advanced age.ConclusionDespite the initial descriptions of COVID-19 being a disease that affects all individuals, regardless of station, our data demonstrate the differential racial effects in the United States. This current pandemic reinforces the need to assess the unequal effects of crises on disadvantaged populations to promote population health.
| S-EPMC7413663 | biostudies-literature
Project description:Many studies have shown that the lysosomal cathepsins, especially cathepsins B/L (CTSB/L) are required for SARS-CoV-2 entry into host cells. Lysosomal proteases, cathepsins are indispensable for normal health and are involved in several brain disorders occurring at different development age periods. On the other hand, it has been well known that COVID-19 infection is largely associated with several neurological disorders. Taken together these findings and given the high levels of expression of CTSB/L in the brain, we here proposed a reasonable hypothesis about the involvement of CTSB/L in the neurological manifestations linked to COVID-19. Pharmacological inhibitions of the CTSB/L could be a potential therapeutic target to block the virus entry as well as to mitigate the brain disorders. To this end, we utilized the network-based drug repurposing analyses to identify the possible drugs that can target CTSB/L. This study identifies the molecules like cyclosporine, phenytoin, and paclitaxel as potential drugs with binding ability to the CTSB/L. Further, we have performed molecular docking and all-atom molecular dynamics (MD) simulations to investigate the stability of CTSL-drug complexes. The results showed strong and stable binding of drugs with CTSL.
| S-EPMC8479516 | biostudies-literature
Project description:In the previous publication "Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?" Conticini et al. hypothesized that the surplus of lethality of the novel SARS-CoV-2 in Northern Italy may be at least in part explained by the evidence of highest pollution reported in this area, as both severe COVID-19 and smog exposure are correlated to an innate immune system hyper-activation with subsequent lung inflammation and injury. Since this hypothesis alone does not fully explain why specific subgroups of patients are at major risk, we hypothesized that obesity may be one of the links between COVID-19 severity and high level of air pollution. First, obesity is a predisposing factor for SARS-Cov-2 infection and worse COVID-19 outcomes, and unequivocal evidence demonstrated that fat mass excess is independently associated with several pulmonary diseases and lung inflammation. Moreover, it has been shown that obesity may intensify the detrimental effects of air pollution on the lungs, and this is not surprising if we consider that these conditions share an excessive activation of the immune system and a lung inflammatory infiltrate. Finally, fat mass excess has also been speculated to be itself a consequence of air pollutants exposure, which has been proved to induce metabolic disruption and weight gain in murine models. In conclusion, although many variables must be taken into account in the analysis of the pandemic, our observations suggest that obesity may act as effect modifier of smog-induced lung-injury, and the concomitant presence of these two factors could better explain the higher virulence, faster spread and greater mortality of SARS-CoV-2 in Northern Italy compared to the rest of the country.
| S-EPMC7397942 | biostudies-literature
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-associated coronavirus disease 2019 (COVID-19) pandemic has been the subject of a large number of studies in recent times. Here, starting from the evidence that in Italy, the areas with the lowest number of COVID-19 cases were those with the highest incidence of malaria in the early 1900's, we explore possible inverse relationships between malaria and COVID-19. Indeed, some genetic variants, which have been demonstrated to give an advantage against malaria, can also play a role in the incidence and severity of SARS-CoV-2 infections (e.g., the ACE2 receptor). To verify this scientific hypothesis, we here use public data from whole-genome sequencing (WGS) experiments to extrapolate the genetic information of 46 world populations with matched COVID-19 data. In particular, we focus on 47 genes, including ACE2 and genes which have previously been reported to play a role in malaria. Only common variants (>5%) in at least 30% of the selected populations were considered, and, for this subset, we correlate the intra-population allele frequency with the COVID-19 data (cases/million inhabitants), eventually pinpointing meaningful variants in 6 genes. This study allows us to distinguish between positive and negative correlations, i.e., variants whose frequency significantly increases with increasing or decreasing COVID-19 cases. Finally, we discuss the possible molecular mechanisms associated with these variants and advance potential therapeutic options, which may help fight and/or prevent COVID-19.
| S-EPMC8107224 | biostudies-literature