Immune Complex-Induced, Nitric Oxide-Mediated Vascular Endothelial Cell Death by Phagocytes Is Prevented with Decoy FcγReceptors

Mula, Ramanjaneya V.R.; Machiah, Deepa; Holland, Lauren; Wang, Xinyu; Parihar, Harish S.; Sharma, Avadhesh C.; Selvaraj, Periasamy; Shashidharamurthy, Rangaiah

doi:10.1371/journal.pone.0153620

Cited by 5 publications

(3 citation statements)

References 57 publications

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“…The released NO in the microenvironment is known to initiate the apoptotic pathway [ 31 ]. In the present study, we found that EV71 infection induced apoptosis and inhibited viability of RD cells.…”

Section: Discussionmentioning

confidence: 99%

Involvement of inducible nitric oxide synthase and mitochondrial dysfunction in the pathogenesis of enterovirus 71 infection

Dang

Zhang

et al. 2017

Oncotarget

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Enterovirus71 (EV71) is recognized as the main causative agent of severe hand, foot and mouth disease (HFMD). However, the pathogenesis of EV71 infection has not been well characterized. Clinical evidence indicated that inducible nitric oxide synthase (iNOS) induction in the lung of HFMD patients contributes to the severe symptoms of pulmonary edema. In the present study, we recruited 142 subjects including HFMD patients and controls, and serum level of nitric oxide (NO) was determined. Next, cellular and animal model were used to further investigate the roles of iNOS and mitochondria damage during EV71 infection. Serum NO level in HFMD patients with mild or severe symptoms was higher than that in controls, and there was a trend towards an increase in the serum NO level of severe cases relative to mild cases. EV71 infection caused apoptosis and increased levels of NO, iNOS, superoxide dismutase (SOD) activity and malondialdehyde (MDA), and degraded mitochondrial membrane potential (ΔΨm) in vitro. Pathological alterations of mitochondrial morphology were observed in vitro and in vivo. Furthermore, the expression of iNOS levels in target organs including brain, spinal cord, skeletal muscle, lung and heart were increased with the progression of the pathogenesis of EV71 infection in mice. Taken together, iNOS and mitochondrial damage participate in the pathogenesis of EV71 infection.

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Section: Discussionmentioning

confidence: 99%

Involvement of inducible nitric oxide synthase and mitochondrial dysfunction in the pathogenesis of enterovirus 71 infection

Dang

Zhang

et al. 2017

Oncotarget

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“…Foreign researchers have also found that circulating immune complexes can be deposited in the subendothelial region and damage endothelial cells, causing autoimmune vasculitis (Wang & Law, 2019), and endothelial cell damage occurs as a result of the interaction of immune complexes with Fcgamma receptors (FcγR) expressed on inflammatory cells. At the same time, nitric oxide (NO) induced by immune complexes is one of the main mediators of inflammation that contributes to vascular inflammation and endothelial cell death in immune complex vasculitis (Mula et al, 2016). However, according to other authors (Xu et al, 2022), endothelial cell damage is associated not only with the deposition of immune complexes, but also with complement activation, inflammatory factors and chemokines, oxidative stress, haemodynamic, and coagulation factors.…”

Section: Resultsmentioning

confidence: 99%

Morphological changes in the small intestine mesentery of cats with infectious peritonitis

Borisevich,

Dzimira,

Lisova

et al. 2023

Ukrainian journal of veterinary sciences

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The research relevance is determined by an insufficient study of morphological changes in the mesentery of cats with infectious peritonitis, even though their understanding is necessary to explain the mechanism of development of the main symptom of the disease – the effusion of fluid into the abdominal cavity. The research aims to establish gross and microscopic changes in the mesentery of the small intestine of cats with infectious peritonitis. The research employs gross and histological examination of the mesentery of the small intestine of cats at the infectious peritonitis. Slides of the mesentery were stained with haematoxylin and eosin. At dry and mixed forms of infectious peritonitis, gross and microscopic changes in the mesentery of the small intestine of cats are similar. In the mesentery grossly, small white spots were found, which protruded above the general surface and had a homogeneous appearance on the section. Microscopic changes in the mesentery of the small intestine of cats with dry and mixed forms of infectious peritonitis were also similar. When conducting histological studies, it was established that the mesothelium on the surface of the mesentery was necrotized or absent. The submesothelial layer of collagen fibres was necrotized or contained partially lysed and fragmented fibres. The loose fibrous connective tissue of the mesentery was swollen, necrotized in places, and infiltrated by lymphocytes, monocytes, and macrophages. Eosinophilic inclusion bodies were detected in the cytoplasm of some monocytes and macrophages. Foci of adipose tissue in the mesentery of the small intestine were infiltrated by lymphocytes and monocytes. Necrosis and destruction of their walls were found in blood vessels and destruction of endothelial cells in lymphatic vessels. Perivascular lymphoid nodules were markedly enlarged due to their swelling and an increase in the number of cells in them. In perivascular lymphoid nodules, expansion of lymphatic vessels and destruction of part of their endothelium cells were also established. Some of the lymphatic vessels of the mesentery were expanded and filled with lymph, which contained a significant number of lymphocytes, monocytes, and single neutrophils. The materials presented in the article are of practical value for anatomists, histologists and pathomorphologists, as well as for scientists who study the pathogenesis of infectious peritonitis in cats

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“…In organs such as the heart, brain, and kidney, failure is associated with high mortality. Vasculitis, a common presentation in lupus patients, arises when direct antibodies against endothelial cells as well antigen-antibodies complex become deposited in blood vessels [ 114 , 115 ]; it could also arise due to vasculitis in situ. Vasculitis aggravates the state of endothelial dysfunction with the rapid development of premature atherosclerosis [ 12 , 44 ].…”

Section: The Effect Of Airds On Vascular Function (Premature Atherosclerosis)mentioning

confidence: 99%

Autoimmune Rheumatic Diseases and Vascular Function: The Concept of Autoimmune Atherosclerosis

Hedar

Stradner

Roessler

et al. 2021

JCM

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Autoimmune rheumatic diseases (AIRDs) with unknown etiology are increasing in incidence and prevalence. Up to 5% of the population is affected. AIRDs include rheumatoid arthritis, system lupus erythematosus, systemic sclerosis, and Sjögren’s syndrome. In patients with autoimmune diseases, the immune system attacks structures of its own body, leading to widespread tissue and organ damage, which, in turn, is associated with increased morbidity and mortality. One third of the mortality associated with autoimmune diseases is due to cardiovascular diseases. Atherosclerosis is considered the main underlying cause of cardiovascular diseases. Currently, because of finding macrophages and lymphocytes at the atheroma, atherosclerosis is considered a chronic immune-inflammatory disease. In active inflammation, the liberation of inflammatory mediators such as tumor necrotic factor alpha (TNFa), interleukine-6 (IL-6), IL-1 and other factors like T and B cells, play a major role in the atheroma formation. In addition, antioxidized, low-density lipoprotein (LDL) antibodies, antinuclear antibodies (ANA), and rheumatoid factor (RF) are higher in the atherosclerotic patients. Traditional risk factors like gender, age, hypercholesterolemia, smoking, diabetes mellitus, and hypertension, however, do not alone explain the risk of atherosclerosis present in autoimmune diseases. This review examines the role of chronic inflammation in the etiology—and progression—of atherosclerosis in autoimmune rheumatic diseases. In addition, discussed here in detail are the possible effects of autoimmune rheumatic diseases that can affect vascular function. We present here the current findings from studies that assessed vascular function changes using state-of-the-art techniques and innovative endothelial function biomarkers.

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Immune Complex-Induced, Nitric Oxide-Mediated Vascular Endothelial Cell Death by Phagocytes Is Prevented with Decoy FcγReceptors

Cited by 5 publications

References 57 publications

Involvement of inducible nitric oxide synthase and mitochondrial dysfunction in the pathogenesis of enterovirus 71 infection

Involvement of inducible nitric oxide synthase and mitochondrial dysfunction in the pathogenesis of enterovirus 71 infection

Morphological changes in the small intestine mesentery of cats with infectious peritonitis

Autoimmune Rheumatic Diseases and Vascular Function: The Concept of Autoimmune Atherosclerosis

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