scholarly journals Access to the Spleen Microenvironment through Lymph Shows Local Cytokine Production, Increased Cell Flux, and Altered Signaling of Immune Cells during Lipopolysaccharide-Induced Acute Inflammation

2010 ◽  
Vol 184 (8) ◽  
pp. 4547-4556 ◽  
Author(s):  
Elvira Semaeva ◽  
Olav Tenstad ◽  
Jørn Skavland ◽  
Marianne Enger ◽  
Per Ole Iversen ◽  
...  
Keyword(s):  
Immune Cells ◽  
Acute Inflammation ◽  
Cytokine Production ◽  
Local Cytokine

252 Hepatitis C virus impairs cytokine production by immune cells

Cytokine ◽  
2008 ◽  
Vol 43 (3) ◽  
pp. 299
Author(s):  
Marie-Eve Bilodeau ◽  
Emmanuel Moreau ◽  
Esther Tarrab ◽  
Alain Lamarre
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Immune Cells ◽  
Cytokine Production

scholarly journals Local sympathetic neurons promote neutrophil egress from the bone marrow at the onset of acute inflammation

2020 ◽  
Vol 32 (11) ◽  
pp. 727-736 ◽  
Author(s):  
Tomoka Ao ◽  
Junichi Kikuta ◽  
Takao Sudo ◽  
Yutaka Uchida ◽  
Kenta Kobayashi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Immune Cells ◽  
Acute Inflammation ◽  
Sympathetic Neurons ◽  
Dependent Manner ◽  
Adrenergic Signaling ◽  
Sympathetic Nervous

Abstract The sympathetic nervous system plays critical roles in the differentiation, maturation and recruitment of immune cells under homeostatic conditions, and in responses to environmental stimuli, although its role in the migratory control of immune cells during acute inflammation remains unclear. In this study, using an advanced intravital bone imaging system established in our laboratory, we demonstrated that the sympathetic nervous system locally regulates neutrophil egress from the bone marrow for mobilization to inflammatory foci. We found that sympathetic neurons were located close to blood vessels in the bone marrow cavity; moreover, upon lipopolysaccharide (LPS) administration, local sympathectomy delayed neutrophil egress from the bone marrow and increased the proportion of neutrophils that remained in place. We also showed that vascular endothelial cells produced C-X-C motif chemokine ligand 1 (CXCL1), which is responsible for neutrophil egress out of the bone marrow. Its expression was up-regulated during acute inflammation, and was suppressed by β-adrenergic receptor blockade, which was accompanied with inhibition of neutrophil egress into the systemic circulation. Furthermore, systemic β-adrenergic signaling blockade decreased the recruitment of neutrophils in the lung under conditions of acute systemic inflammation. Taken together, the results of this study first suggested a new regulatory system, wherein local sympathetic nervous activation promoted neutrophil egress by enhancing Cxcl1 expression in bone marrow endothelial cells in a β-adrenergic signaling-dependent manner, contributing to the recruitment of neutrophils at the onset of inflammation in vivo.

scholarly journals TCT-157 Increased Local Cytokine Production at Culprit Superficial Femoral Artery Plaques

2012 ◽  
Vol 60 (17) ◽  
pp. B45-B46
Author(s):  
Cameron Donaldson ◽  
David Schneider ◽  
Daniel Bertges ◽  
Julie Adams ◽  
Nader Elgharib ◽  
...  
Keyword(s):  
Femoral Artery ◽  
Superficial Femoral Artery ◽  
Cytokine Production ◽  
Local Cytokine

Exacerbates kidney injury in mice subjected to sepsis: critical impact of used heparin

2018 ◽  
Vol 6 (4) ◽  
pp. 323-335
Author(s):  
Peter Weighardt ◽  
Niels Hayashi
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Cytokine Production ◽  
Multiorgan Failure ◽  
Kidney Injury ◽  
Tubular Dysfunction ◽  
Cytokine Storm ◽  
Peritubular Capillary ◽  
Inflammatory Reactions ◽  
Local Cytokine

Sepsis is the leading cause of death in critically ill patients, and the incidence of sepsis is increasing causes multiorgan failure, including acute kidney injury (AKI) and patients with both sepsis and AKI have an especially high mortality rate. Several different pathophysiological mechanisms have been proposed for sepsis-induced AKI: vasodilation-induced glomerular hypoperfusion, dysregulated circulation within the peritubular capillary network, inflammatory reactions by systemic cytokine storm or local cytokine production, and tubular dysfunction induced by oxidative stress animal sepsis models have been developed using LPS infusion. Renal dysfunction evaluated by serum creatinine and BUN was found in acute non-survivors (<24 hours) and decreased urine output in subacute non-survivors (24–96 hours). The study show that increased AKI in animal with blood collected heparin (P=0.002) compared to citrate, furthermore; sham mice that received heparin did not develop AKI.

scholarly journals Opioids and clonidine modulate cytokine production and opioid receptor expression in neonatal immune cells

2012 ◽  
Vol 33 (5) ◽  
pp. 374-382 ◽  
Author(s):  
R Chavez-Valdez ◽  
L Kovell ◽  
R Ahlawat ◽  
G L McLemore ◽  
M Wills-Karp ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Immune Cells ◽  
Cytokine Production ◽  
Receptor Expression
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