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1.
Hamostaseologie ; 41(5): 387-396, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1483190

ABSTRACT

Hypercoagulability and vascular injury, which characterize morbidity in COVID-19 disease, are frequently observed in the skin. Several pathomechanisms, such as inflammation caused by angiotensin-converting enzyme 2-mediated uptake into endothelial cells or SARS-CoV-2-initiated host immune responses, contribute to microthrombus formation and the appearance of vascular skin lesions. Besides pathophysiologic mechanisms observed in the skin, this review describes the clinical appearance of cutaneous vascular lesions and their association with COVID-19 disease, including acro-ischemia, reticular lesions, and cutaneous small vessel vasculitis. Clinicians need to be aware that skin manifestations may be the only symptom in SARS-CoV-2 infection, and that inflammatory and thrombotic SARS-CoV-2-driven processes observed in multiple organs and tissues appear identically in the skin as well.


Subject(s)
COVID-19/complications , SARS-CoV-2 , Skin/blood supply , Angiotensin-Converting Enzyme 2/physiology , Antibodies, Antiphospholipid/blood , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/pathology , COVID-19/pathology , COVID-19/physiopathology , Complement Activation , Cytokines/metabolism , Host Microbial Interactions/immunology , Host Microbial Interactions/physiology , Humans , Microvessels/immunology , Microvessels/pathology , Microvessels/physiopathology , Pandemics , SARS-CoV-2/pathogenicity , SARS-CoV-2/physiology , Skin/immunology , Vasculitis/etiology , Vasculitis/pathology , Vasculitis/physiopathology , Virus Internalization
2.
Pharmacol Res ; 168: 105581, 2021 06.
Article in English | MEDLINE | ID: covidwho-1157664

ABSTRACT

In-depth characterization of heart-brain communication in critically ill patients with severe acute respiratory failure is attracting significant interest in the COronaVIrus Disease 19 (COVID-19) pandemic era during intensive care unit (ICU) stay and after ICU or hospital discharge. Emerging research has provided new insights into pathogenic role of the deregulation of the heart-brain axis (HBA), a bidirectional flow of information, in leading to severe multiorgan disease syndrome (MODS) in patients with confirmed infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Noteworthy, HBA dysfunction may worsen the outcome of the COVID-19 patients. In this review, we discuss the critical role HBA plays in both promoting and limiting MODS in COVID-19. We also highlight the role of HBA as new target for novel therapeutic strategies in COVID-19 in order to open new translational frontiers of care. This is a translational perspective from the Italian Society of Cardiovascular Researches.


Subject(s)
Brain Diseases/therapy , Brain/drug effects , COVID-19/therapy , Heart Diseases/therapy , Heart/drug effects , Adrenal Cortex Hormones/administration & dosage , Anti-Inflammatory Agents/administration & dosage , Antiviral Agents/administration & dosage , Brain/immunology , Brain/metabolism , Brain Diseases/immunology , Brain Diseases/metabolism , COVID-19/immunology , COVID-19/metabolism , Critical Care/methods , Critical Illness/therapy , Dietary Supplements , Functional Food , Heart Diseases/immunology , Heart Diseases/metabolism , Humans , Inflammation Mediators/antagonists & inhibitors , Inflammation Mediators/immunology , Inflammation Mediators/metabolism , Microvessels/drug effects , Microvessels/immunology , Microvessels/metabolism , Multiple Organ Failure/immunology , Multiple Organ Failure/metabolism , Multiple Organ Failure/therapy , SARS-CoV-2/drug effects , SARS-CoV-2/immunology , SARS-CoV-2/metabolism
3.
Scand J Immunol ; 93(6): e13024, 2021 Jun.
Article in English | MEDLINE | ID: covidwho-1091011

ABSTRACT

Early airway responses to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection are of interest since they could decide whether coronavirus disease-19 (COVID-19) will proceed to life-threatening pulmonary disease stages. Here I discuss endothelial-epithelial co-operative in vivo responses producing first-line, humoral innate defence opportunities in human airways. The pseudostratified epithelium of human nasal and tracheobronchial airways are prime sites of exposure and infection by SARS-CoV-2. Just beneath the epithelium runs a profuse systemic microcirculation. Its post-capillary venules respond conspicuously to mucosal challenges with autacoids, allergens and microbes, and to mere loss of epithelium. By active venular endothelial gap formation, followed by transient yielding of epithelial junctions, non-sieved plasma macromolecules move from the microcirculation to the mucosal surface. Hence, plasma-derived protein cascade systems and antimicrobial peptides would have opportunity to operate jointly on an unperturbed mucosal lining. Similarly, a plasma-derived, dynamic gel protects sites of epithelial sloughing-regeneration. Precision for this indiscriminate humoral molecular response lies in restricted location and well-regulated duration of plasma exudation. Importantly, the endothelial responsiveness of the airway microcirculation differs distinctly from the relatively non-responsive, low-pressure pulmonary microcirculation that non-specifically, almost irreversibly, leaks plasma in life-threatening COVID-19. Observations in humans of infections with rhinovirus, coronavirus 229E, and influenza A and B support a general but individually variable early occurrence of plasma exudation in human infected nasal and tracheobronchial airways. Investigations are warranted to elucidate roles of host- and drug-induced airway plasma exudation in restriction of viral infection and, specifically, whether it contributes to variable disease responses following exposure to SARS-CoV-2.


Subject(s)
COVID-19/immunology , COVID-19/virology , Host-Pathogen Interactions/immunology , Immunity, Humoral , Respiratory Mucosa/immunology , Respiratory Mucosa/virology , SARS-CoV-2/immunology , Antibodies, Viral/blood , Antibodies, Viral/immunology , Biomarkers/blood , Blood Proteins , COVID-19/diagnosis , COVID-19/metabolism , Capillary Permeability/immunology , Complement Activation/immunology , Complement System Proteins/immunology , Complement System Proteins/metabolism , Exudates and Transudates , Humans , Immunity, Innate , Immunoglobulin M/blood , Immunoglobulin M/immunology , Microvessels/immunology , Microvessels/metabolism , Respiratory Mucosa/metabolism
4.
Fluids Barriers CNS ; 17(1): 55, 2020 Sep 10.
Article in English | MEDLINE | ID: covidwho-755214

ABSTRACT

Human coronaviruses are highly pathogenic viruses that pose a serious threat to human health. Examples include the severe acute respiratory syndrome outbreak of 2003 (SARS-CoV-1), the Middle East Respiratory Syndrome (MERS-CoV) outbreak of 2012, and the current SARS-CoV-2 (COVID-19) pandemic. Herein, we review the neurological manifestations of coronaviruses and discuss the potential pathogenic role of blood-brain barrier dysfunction. We present the hypothesis that pre-existing vascular damage (due to aging, cardiovascular disease, diabetes, hypertension or other conditions) facilitates infiltration of the virus into the central nervous system (CNS), increasing neuro-inflammation and the likelihood of neurological symptoms. We also discuss the role of a neuroinflammatory cytokine profile in both blood-brain barrier dysfunction and macrovascular disease (e.g. ischemic stroke and thromboembolism). Future studies are needed to better understand the involvement of the microvasculature in coronavirus neuropathology, and to test the diagnostic potential of minimally-invasive screening tools (e.g. serum biomarkers, fluorescein retinal angiography and dynamic-contrast MRI).


Subject(s)
Blood-Brain Barrier/physiopathology , Coronavirus Infections/physiopathology , Inflammation/physiopathology , Microvessels/physiopathology , Nervous System Diseases/physiopathology , Pneumonia, Viral/physiopathology , Betacoronavirus , Blood-Brain Barrier/immunology , Blood-Brain Barrier/virology , COVID-19 , Cardiovascular Diseases/physiopathology , Coronavirus Infections/immunology , Cytokines/immunology , Diabetes Mellitus/physiopathology , Encephalitis/immunology , Encephalitis/physiopathology , Humans , Inflammation/immunology , Microvessels/immunology , Nervous System Diseases/immunology , Pandemics , Pneumonia, Viral/immunology , SARS-CoV-2 , Seizures/immunology , Seizures/physiopathology , Stroke/immunology , Stroke/physiopathology , Thromboembolism/immunology , Thromboembolism/physiopathology
5.
ACS Chem Neurosci ; 11(14): 2048-2050, 2020 07 15.
Article in English | MEDLINE | ID: covidwho-627315

ABSTRACT

In COVID-19, lung manifestations present as a slowly evolving pneumonia with insidious early onset interstitial pulmonary edema that undergoes acute exacerbation in the late stages and microvascular thrombosis. Currently, these manifestations are considered to be only consequences of pulmonary SARS-CoV-2 virus infection. We are proposing a new hypothesis that neurogenic insult may also play a major role in the pathogenesis of these manifestations. SARS-CoV-2 mediated inflammation of the nucleus tractus solitarius (NTS) may play a role in the acute exacerbation of pulmonary edema and microvascular clotting in COVID-19 patients.


Subject(s)
Coronavirus Infections/physiopathology , Hypotension/physiopathology , Lung/blood supply , Microvessels/physiopathology , Pneumonia, Viral/physiopathology , Pulmonary Edema/physiopathology , Solitary Nucleus/physiopathology , Thrombosis/physiopathology , Betacoronavirus , COVID-19 , Capillary Permeability/physiology , Coronavirus Infections/immunology , Cytokine Release Syndrome/immunology , Cytokine Release Syndrome/physiopathology , Facial Nerve , Glossopharyngeal Nerve , Humans , Inflammation , Lung/immunology , Microvessels/immunology , Pandemics , Parasympathetic Nervous System/physiopathology , Pneumonia, Viral/immunology , Pulmonary Edema/immunology , SARS-CoV-2 , Solitary Nucleus/immunology , Vagus Nerve , Vasoconstriction
6.
Clin Chim Acta ; 507: 167-173, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-125379

ABSTRACT

Early clinical evidence suggests that severe cases of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), are frequently characterized by hyperinflammation, imbalance of renin-angiotensin-aldosterone system, and a particular form of vasculopathy, thrombotic microangiopathy, and intravascular coagulopathy. In this paper, we present an immunothrombosis model of COVID-19. We discuss the underlying pathogenesis and the interaction between multiple systems, resulting in propagation of immunothrombosis, which through investigation in the coming weeks, may lead to both an improved understanding of COVID-19 pathophysiology and identification of innovative and efficient therapeutic targets to reverse the otherwise unfavorable clinical outcome of many of these patients.


Subject(s)
Aldosterone/immunology , Betacoronavirus/immunology , Coronavirus Infections/immunology , Microvessels/immunology , Pneumonia, Viral/immunology , Renin-Angiotensin System/immunology , Thrombophilia/immunology , Thrombosis/immunology , COVID-19 , Coronavirus Infections/physiopathology , Humans , Immunity, Innate/immunology , Inflammation/immunology , Inflammation/physiopathology , Inflammation/virology , Microvessels/physiopathology , Microvessels/virology , Pandemics , Pneumonia, Viral/physiopathology , SARS-CoV-2 , Thrombophilia/physiopathology , Thrombophilia/virology , Thrombosis/physiopathology , Thrombosis/virology
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