scholarly journals Acute Endotheliitis (Type 3 Hypersensitivity Vasculitis) in Ten COVID-19 Autopsy Brains

2021 ◽  
Author(s):  
Roy H. Rhodes ◽  
Gordon L. Love ◽  
Fernanda Da Silva Lameira ◽  
Maryam Shahmirzadi Sadough ◽  
Sharon E. Fox ◽  
...  
Keyword(s):  
Vascular Endothelial Cell ◽  
Cranial Nerves ◽  
Renin Angiotensin System ◽  
Vascular Wall ◽  
Acute Stage ◽  
Vascular Endothelial ◽  
Cell Infection ◽  
Hypersensitivity Vasculitis ◽  
Antigen Antibody ◽  
Type 3

AbstractCentral nervous system (CNS) involvement in COVID-19 may occur through direct SARS-CoV-2 invasion through peripheral or cranial nerves or through vascular endothelial cell infection. The renin-angiotensin system may play a major part in CNS morbidity. Effects of hypoxia have also been implicated in CNS lesions in COVID-19. This communication reports on ten consecutive autopsies of individuals with death due to COVID-19 with decedent survival ranging from 30 minutes to 84 days after admission. All ten brains examined had neutrophilic microvascular endotheliitis present in variable amounts and variably distributed. Importantly, this acute stage of type 3 hypersensitivity vasculitis can be followed by fibrinoid necrosis and inner vascular wall sclerosis, but these later stages were not found. These results suggest that a vasculitis with autoimmune features occurred in all ten patients. It is possible that viral antigen in or on microvascular walls or other antigen-antibody complexes occurred in all ten patients proximate to death as a form of autoimmune vasculitis.

The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis—ten years later

2020 ◽  
Vol 318 (6) ◽  
pp. L1115-L1130 ◽  
Author(s):  
Carlyne D. Cool ◽  
Wolfgang M. Kuebler ◽  
Harm Jan Bogaard ◽  
Edda Spiekerkoetter ◽  
Mark R. Nicolls ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Treatment Strategies ◽  
Vascular Wall ◽  
Vascular Endothelial ◽  
Proliferating Cells ◽  
Bone Marrow Derived Cells ◽  
Pulmonary Arterial

Severe forms of pulmonary arterial hypertension (PAH) are most frequently the consequence of a lumen-obliterating angiopathy. One pathobiological model is that the initial pulmonary vascular endothelial cell injury and apoptosis is followed by the evolution of phenotypically altered, apoptosis-resistant, proliferating cells and an inflammatory vascular immune response. Although there may be a vasoconstrictive disease component, the increased pulmonary vascular shear stress in established PAH is caused largely by the vascular wall pathology. In this review, we revisit the “quasi-malignancy concept” of severe PAH and examine to what extent the hallmarks of PAH can be compared with the hallmarks of cancer. The cancer model of severe PAH, based on the growth of abnormal vascular and bone marrow-derived cells, may enable the emergence of novel cell-based PAH treatment strategies.

scholarly journals EXPRESS: Mechanisms of SARS-CoV-2 Induced Lung Vascular Disease: Potential Role of Complement

2021 ◽  
pp. 204589402110157
Author(s):  
Kurt R Stenmark ◽  
Maria Frid ◽  
evgenia gerasimovskaya ◽  
hui zhang ◽  
Mary K. McCarthy ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Treatment Options ◽  
Inflammatory Cells ◽  
Vascular Wall ◽  
Assisted Ventilation ◽  
Vascular Involvement ◽  
Vascular Endothelial ◽  
Cell Infection ◽  
Underlying Mechanisms

ABSTRACT: The outbreak of COVID-19 disease, caused by SARS-CoV-2 beta-coronovirus, urges a focused search for the underlying mechanisms and treatment options. The lung is the major target organ of COVID-19, wherein the primary cause of mortality is hypoxic respiratory failure, resulting from acute respiratory disease syndrome (ARDS), with severe hypoxemia, often requiring assisted ventilation. While similar in some ways to ARDS secondary to other causes, lungs of some patients dying with COVID-19 exhibit distinct features of vascular involvement, including severe endothelial injury and cell death via apoptosis and/or pyroptosis, widespread capillary inflammation and thrombosis. Furthermore, the pulmonary pathology of COVID-19 is characterized by focal inflammatory cell infiltration, impeding alveolar gas exchange resulting in areas of local tissue hypoxia, consistent with potential amplification of COVID-19 pathogenicity by hypoxia. Vascular endothelial cells play essential roles in both innate and adaptive immune responses, and are considered to be “conditional innate immune cells” centrally participating in various inflammatory, immune pathologies. Activated endothelial cells produce cytokines/chemokines, dynamically recruit and activate inflammatory cells and platelets, and centrally participate in pro-thrombotic processes (thrombotic microangiopathies). Initial reports presented pathological findings of localized direct infection of vascular endothelial cells with SARS-CoV-2, yet emerging evidence does not support direct infection of endothelial or other vascular wall cell and thus widespread endothelial cell dysfunction and inflammation may be better explained as secondary responses to epithelial cell infection and inflammation. Endothelial cells are also actively engaged in a cross-talk with the complement system, the essential arm of innate immunity. Recent reports present evidence for complement deposition in SARS-CoV-2-damaged lung microcirculation, further strengthening the idea that, in severe cases of COVID-19, complement activation is an essential player, generating destructive hemorrhagic, capillariitis-like tissue damage, clotting, and hyper-inflammation. Thus, complement-targeted therapies are actively in development. This review is intended to explore in detail these ideas.

Effect of angiotensin(1-7) on the expression of E-selectin induced by angiotensinII and its mechanism in vascular endothelial cell

2010 ◽  
Vol 34 (8) ◽  
pp. S71-S71
Author(s):  
Xiaohui Shen ◽  
Zhi‑Bin Wen ◽  
Na Li ◽  
Qingmei Cheng ◽  
Xiaofan He ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

scholarly journals Uric acid promotes oxidative stress and enhances vascular endothelial cell apoptosis in rats with middle cerebral artery occlusion

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Chengfu Song ◽  
Xiangdong Zhao
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cell ◽  
Artery Occlusion ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Related Factors ◽  
Cerebral Artery Occlusion

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.

scholarly journals Role of the retinal vascular endothelial cell in ocular disease

2013 ◽  
Vol 32 ◽  
pp. 102-180 ◽  
Author(s):  
Arpita S. Bharadwaj ◽  
Binoy Appukuttan ◽  
Phillip A. Wilmarth ◽  
Yuzhen Pan ◽  
Andrew J. Stempel ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Ocular Disease ◽  
Vascular Endothelial ◽  
Retinal Vascular Endothelial Cell
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