Diabetes, infection risk and COVID-19

Erener, Süheda

doi:10.1016/j.molmet.2020.101044

Cited by 261 publications

(259 citation statements)

References 126 publications

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“…Third, superinfection, which represents a new albeit scarcely studied condition in COVID-19 [5], particularly for invasive fungal infections [14,29]. The peculiar pathophysiology of either diabetes [11] or COVID-19 [30] may account for the occurrence of bacterial and fungal coinfections in our case, as in other cases [3,31]. The diabetes-induced immune dysregulation may exacerbate the virus-activated hyper-inflammatory "cytokine storm", which in turn leads to complications (e.g., ARDS, shock, multiorgan failure and death) seen in severe COVID-19 phases [10].…”

Section: Discussionmentioning

confidence: 99%

Pan-Echinocandin-Resistant Candida glabrata Bloodstream Infection Complicating COVID-19: A Fatal Case Report

Posteraro

Torelli

Vella

et al. 2020

JoF

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Coinfections with bacteria or fungi may be a frequent complication of COVID-19, but coinfections with Candida species in COVID-19 patients remain rare. We report the 53-day clinical course of a complicated type-2 diabetes patient diagnosed with COVID-19, who developed bloodstream infections initially due to methicillin-resistant Staphylococcus aureus, secondly due to multidrug-resistant Gram-negative bacteria, and lastly due to a possibly fatal Candida glabrata. The development of FKS-associated pan-echinocandin resistance in the C. glabrata isolated from the patient after 13 days of caspofungin treatment aggravated the situation. The patient died of septic shock shortly before the prospect of receiving potentially effective antifungal therapy. This case emphasizes the importance of early diagnosis and monitoring for antimicrobial drug-resistant coinfections to reduce their unfavorable outcomes in COVID-19 patients.

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Section: Discussionmentioning

confidence: 99%

Pan-Echinocandin-Resistant Candida glabrata Bloodstream Infection Complicating COVID-19: A Fatal Case Report

Posteraro

Torelli

Vella

et al. 2020

JoF

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“…The coherence between obesity, diabetes, and COVID-19 is suggested at least by five different factors: viral load, immune response, alveolar dysfunction, endothelial dysfunction, and coagulopathy [189]. As ACE2 mediates the entry of SARS-CoV-2 into the host cells, and an increased expression of ACE2 was detected in lung, kidney, and heart tissue of diabetic mice [190], diabetes could foster the viral load in COVID-19 patients.…”

Section: Obesity Diabetes and Their Implications In Covid-19mentioning

confidence: 99%

“…As ACE2 mediates the entry of SARS-CoV-2 into the host cells, and an increased expression of ACE2 was detected in lung, kidney, and heart tissue of diabetic mice [190], diabetes could foster the viral load in COVID-19 patients. Next, the immune response is altered in patients with obesity and diabetes, both factors are associated with a chronic low-level inflammation [11,191], reduced NK cell activity, and deregulated numbers of CD4 + and CD8 + T cells [189], which could cause a delayed immune response and a prolonged hyperinflammation in COVID-19 patients. Moreover, molecular mechanisms of impaired endothelium in patients with diabetes are complex and connected to oxidative stress, inflammation, and a change in the hemodynamic balance [82].…”

Section: Obesity Diabetes and Their Implications In Covid-19mentioning

confidence: 99%

Obesity and COVID-19: Molecular Mechanisms Linking Both Pandemics

Ritter

Kreis

Louwen

et al. 2020

IJMS

109

114

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The coronavirus disease 2019 COVID-19 pandemic is rapidly spreading worldwide and is becoming a major public health crisis. Increasing evidence demonstrates a strong correlation between obesity and the COVID-19 disease. We have summarized recent studies and addressed the impact of obesity on COVID-19 in terms of hospitalization, severity, mortality, and patient outcome. We discuss the potential molecular mechanisms whereby obesity contributes to the pathogenesis of COVID-19. In addition to obesity-related deregulated immune response, chronic inflammation, endothelium imbalance, metabolic dysfunction, and its associated comorbidities, dysfunctional mesenchymal stem cells/adipose-derived mesenchymal stem cells may also play crucial roles in fueling systemic inflammation contributing to the cytokine storm and promoting pulmonary fibrosis causing lung functional failure, characteristic of severe COVID-19. Moreover, obesity may also compromise motile cilia on airway epithelial cells and impair functioning of the mucociliary escalators, reducing the clearance of severe acute respiratory syndrome coronavirus (SARS-CoV-2). Obese diseased adipose tissues overexpress the receptors and proteases for the SARS-CoV-2 entry, implicating its possible roles as virus reservoir and accelerator reinforcing violent systemic inflammation and immune response. Finally, anti-inflammatory cytokines like anti-interleukin 6 and administration of mesenchymal stromal/stem cells may serve as potential immune modulatory therapies for supportively combating COVID-19. Obesity is conversely related to the development of COVID-19 through numerous molecular mechanisms and individuals with obesity belong to the COVID-19-susceptible population requiring more protective measures.

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“…71 Obesity and diabetes are known to increase the risk of mortality and severe complications resulting from respiratory infection, [72][73][74] including the novel coronavirus SARS-CoV-2. 75 Epidemiological evidence suggests dyslipidemia itself-both abnormally low or high cholesterol levels-is associated with heightened susceptibility to acute infection as well, although causality has not yet been proven clinically. 76,77 Mouse models of spontaneous hypercholesterolaemia have demonstrated that dyslipidemia increases susceptibility to infections by pathogens such as Mycobacterium tuberculosis, 78 Listeria monocytogenes 79 and Leishmania major.…”

Section: Dyslipidemia and Immune Cell Motilitymentioning

confidence: 99%

Implications of cellular metabolism for immune cell migration

Guak

Krawczyk

2020

Immunology

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Cell migration is an essential, energetically demanding process in immunity. Immune cells navigate the body via chemokines and other immune mediators, which are altered under inflammatory conditions of injury or infection. Several factors determine the migratory abilities of different types of immune cells in diverse contexts, including the precise coordination of cytoskeletal remodelling, the expression of specific chemokine receptors and integrins, and environmental conditions. In this review, we present an overview of recent advances in our understanding of the relationship of each of these factors with cellular metabolism, with a focus on the spatial organization of glycolysis and mitochondria, reciprocal regulation of chemokine receptors and the influence of environmental changes.

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Diabetes, infection risk and COVID-19

Cited by 261 publications

References 126 publications

Pan-Echinocandin-Resistant Candida glabrata Bloodstream Infection Complicating COVID-19: A Fatal Case Report

Pan-Echinocandin-Resistant Candida glabrata Bloodstream Infection Complicating COVID-19: A Fatal Case Report

Obesity and COVID-19: Molecular Mechanisms Linking Both Pandemics

Implications of cellular metabolism for immune cell migration

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