LPS-induced expression and release of monocyte tissue factor in patients with haemophilia

Holstein, Katharina; Matysiak, Anna; Witt, Leonora; Sievers, Bianca; Beckmann, Lennart; Haddad, Munif; Renné, Thomas; Voigtlaender, Minna

doi:10.1007/s00277-020-04075-6

Cited by 6 publications

(4 citation statements)

References 42 publications

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“…The extrinsic coagulation cascade can be triggered by soluble or cell-surface CD142 (tissue factor). Prior studies have demonstrated increased CD142 expression in the setting of viral infections (55-58) and in response to LPS (55, 59). In addition, there is a correlation between higher levels of CD142 and COVID-19 disease severity (57, 58).…”

Section: Expression Of Cd142 (Tissue Factor) Is Decreased In Convales...mentioning

confidence: 99%

Reduced monocyte proportions and responsiveness in convalescent COVID-19 patients

Ravkov,

Williams,

Elgort

et al. 2024

Front. Immunol.

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IntroductionThe clinical manifestations of acute severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection and coronavirus disease 2019 (COVID-19) suggest a dysregulation of the host immune response that leads to inflammation, thrombosis, and organ dysfunction. It is less clear whether these dysregulated processes persist during the convalescent phase of disease or during long COVID. We sought to examine the effects of SARS-CoV-2 infection on the proportions of classical, intermediate, and nonclassical monocytes, their activation status, and their functional properties in convalescent COVID-19 patients.MethodsPeripheral blood mononuclear cells (PBMCs) from convalescent COVID-19 patients and uninfected controls were analyzed by multiparameter flow cytometry to determine relative percentages of total monocytes and monocyte subsets. The expression of activation markers and proinflammatory cytokines in response to LPS treatment were measured by flow cytometry and ELISA, respectively.ResultsWe found that the percentage of total monocytes was decreased in convalescent COVID-19 patients compared to uninfected controls. This was due to decreased intermediate and non-classical monocytes. Classical monocytes from convalescent COVID-19 patients demonstrated a decrease in activation markers, such as CD56, in response to stimulation with bacterial lipopolysaccharide (LPS). In addition, classical monocytes from convalescent COVID-19 patients showed decreased expression of CD142 (tissue factor), which can initiate the extrinsic coagulation cascade, in response to LPS stimulation. Finally, we found that monocytes from convalescent COVID-19 patients produced less TNF-α and IL-6 in response to LPS stimulation, than those from uninfected controls.ConclusionSARS-CoV-2 infection exhibits a clear effect on the relative proportions of monocyte subsets, the activation status of classical monocytes, and proinflammatory cytokine production that persists during the convalescent phase of disease.

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Section: Expression Of Cd142 (Tissue Factor) Is Decreased In Convales...mentioning

confidence: 99%

Reduced monocyte proportions and responsiveness in convalescent COVID-19 patients

Ravkov,

Williams,

Elgort

et al. 2024

Front. Immunol.

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“…The extrinsic coagulation cascade can be triggered by soluble or cell-surface CD142 (tissue factor). Prior studies have demonstrated increased CD142 expression in the setting of viral infections [49][50][51][52] and in response to LPS 49,53 . In addition, there is a correlation between higher levels of CD142 and COVID-19 disease severity 51,52 .…”

Section: Expression Of Cd142 (Tissue Factor) Is Decreased In Convales...mentioning

confidence: 99%

Reduced Monocyte Proportions and Responsiveness in Convalescent COVID-19 Patients

Ravkov,

Williams,

Elgort

et al. 2023

Preprint

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The clinical manifestations of acute severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection and COVID-19 suggest a dysregulation of the host immune response that leads to inflammation, thrombosis, and organ dysfunction. It is less clear whether these dysregulated processes persist during the convalescent phase of disease or during long COVID. We investigated the effects of SARS-CoV-2 infection on the proportions of classical, intermediate, and non-classical monocytes, their activation status, and their functional properties in convalescent COVID-19 patients and uninfected control subjects. We found that the percentage of total monocytes was decreased in convalescent COVID-19 patients compared to uninfected controls. This was due to decreased intermediate and non-classical monocytes. Classical monocytes from convalescent COVID-19 patients demonstrated a decrease in activation markers, such as CD56, in response to stimulation with bacterial lipopolysaccharide (LPS). In addition, classical monocytes from convalescent COVID-19 patients showed decreased expression of CD142 (tissue factor), which can initiate the extrinsic coagulation cascade, in response to LPS stimulation. Finally, we found that monocytes from convalescent COVID-19 patients produced less TNF-α and IL-6 in response to LPS stimulation, than those from uninfected controls. In conclusion, SARS-CoV-2 infection exhibits a clear effect on the relative proportions of monocyte subsets, the activation status of classical monocytes, and proinflammatory cytokine production that persists during the convalescent phase of disease.

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“…Liver cirrhosis patients usually have higher endotoxemia and systemic inflammation due to gut dysbiosis. Endotoxin can increase thrombosis through the production of tissue factor (TF) ( 75 ). With the increase of intestinal permeability and bacterial translocation, the level of LPS in the blood of patients with liver cirrhosis increased significantly.…”

Section: Liver Cirrhosis-related Complications and Dysbiosismentioning

confidence: 99%

Liver cirrhosis and complications from the perspective of dysbiosis

Nie,

Zhang,

Xie

et al. 2024

Front. Med.

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The gut-liver axis refers to the intimate relationship and rigorous interaction between the gut and the liver. The intestinal barrier’s integrity is critical for maintaining liver homeostasis. The liver operates as a second firewall in this interaction, limiting the movement of potentially dangerous compounds from the gut and, as a result, contributing in barrier management. An increasing amount of evidence shows that increased intestinal permeability and subsequent bacterial translocation play a role in liver damage development. The major pathogenic causes in cirrhotic individuals include poor intestinal permeability, nutrition, and intestinal flora dysbiosis. Portal hypertension promotes intestinal permeability and bacterial translocation in advanced liver disease, increasing liver damage. Bacterial dysbiosis is closely related to the development of cirrhosis and its related complications. This article describes the potential mechanisms of dysbiosis in liver cirrhosis and related complications, such as spontaneous bacterial peritonitis, hepatorenal syndrome, portal vein thrombosis, hepatic encephalopathy, and hepatocellular carcinoma, using dysbiosis of the intestinal flora as an entry point.

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LPS-induced expression and release of monocyte tissue factor in patients with haemophilia

Cited by 6 publications

References 42 publications

Reduced monocyte proportions and responsiveness in convalescent COVID-19 patients

Reduced monocyte proportions and responsiveness in convalescent COVID-19 patients

Reduced Monocyte Proportions and Responsiveness in Convalescent COVID-19 Patients

Liver cirrhosis and complications from the perspective of dysbiosis

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