scholarly journals An opposing time-dependent immune-modulating effect of the sympathetic nervous system conferred by altering the cytokine profile in the local lymph nodes and spleen of mice with type II collagen-induced arthritis

2005 ◽  
Vol 52 (4) ◽  
pp. 1305-1313 ◽  
Author(s):  
Peter Härle ◽  
Daniel Möbius ◽  
Daniel J. J. Carr ◽  
Jürgen Schölmerich ◽  
Rainer H. Straub
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Lymph Nodes ◽  
Type Ii Collagen ◽  
Cytokine Profile ◽  
Time Dependent ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Sympathetic Nervous

scholarly journals Dexamethasone Preconditioning Improves the Response of Collagen-Induced Arthritis to Treatment with Short-Term Lipopolysaccharide-Stimulated Collagen-Loaded Dendritic Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Corina Peña ◽  
David Gárate ◽  
Juan Contreras-Levicoy ◽  
Octavio Aravena ◽  
Diego Catalán ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Combined Treatment ◽  
Type Ii Collagen ◽  
Cytokine Profile ◽  
Clinical Disease ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Short Term

Background. Pharmacologically modulated dendritic cells (DCs) have been shown to restore tolerance in type II collagen-(CII-) induced arthritis (CIA). We examined the effect of dexamethasone (DXM) administration as a preconditioning agent, followed by an injection of lipopolysaccharide-(LPS-) stimulated and CII-loaded DCs on the CIA course.Methods. After CIA induction, mice pretreated with DXM were injected with 4-hour LPS-stimulated DCs loaded with CII (DXM/4hLPS/CII/DCs).Results. Mice injected with DXM/4hLPS/CII/DCs displayed significantly less severe clinical disease compared to animals receiving 4hLPS/CII/DCs alone or those in which only DXM was administered. Cytokine profile evaluation showed that CD4+ T cells from DXM/4hLPS/CII/DCs and 4hLPS/CII/DCs groups release higher IL-10 levels than those from mice receiving DXM alone or CIA mice. CD4+ T cells from all DC-treated groups showed less IL-17 release when compared to the CIA group. On the contrary, CD4+ T cells from DXM/4hLPS/CII/DCs and 4hLPS/CII/DCs groups released higher IFN-γlevels than those from CIA group.Conclusion. A combined treatment, including DXM preconditioning followed by an inoculation of short-term LPS-stimulated CII-loaded DCs, provides an improved strategy for attenuating CIA severity. Our results suggest that this benefit is driven by a modulation in the cytokine profile secreted by CD4+ T cells.

scholarly journals An early sympathetic nervous system influence exacerbates collagen-induced arthritis via CD4+CD25+ cells

2008 ◽  
Vol 58 (8) ◽  
pp. 2347-2355 ◽  
Author(s):  
Peter Härle ◽  
Georg Pongratz ◽  
Julia Albrecht ◽  
Ingo H. Tarner ◽  
Rainer H. Straub
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Collagen Induced Arthritis ◽  
Sympathetic Nervous

scholarly journals Prevention of type II collagen-induced arthritis by in vivo treatment with anti-L3T4.

1985 ◽  
Vol 162 (3) ◽  
pp. 1105-1110 ◽  
Author(s):  
G E Ranges ◽  
S Sriram ◽  
S M Cooper
Keyword(s):  
T Cells ◽  
Lymph Nodes ◽  
Humoral Response ◽  
Type Ii Collagen ◽  
Type Ii ◽  
Collagen Induced Arthritis ◽  
Delayed Onset ◽  
Treatment Administration ◽  
In Vivo Administration

The effect of in vivo administration of monoclonal anti-L3T4 antibody on the development of murine collagen-induced arthritis (CIA) was assessed. Treatment with anti-L3T4 resulted in a greater than 90% depletion of L3T4+ T cells in lymph nodes and spleen, an effect that appears entirely reversed 30 d after treatment. Administration of anti-L3T4 before immunization with type II collagen resulted in a significant decrease in arthritis incidence and delayed onset of the disease while treatment begun after a strong anticollagen IgG humoral response was underway was not effective in altering disease expression. These results suggest a prominent role for L3T4+ T cells in the pathogenesis of CIA.

Control of pulmonary surfactant secretion from type II pneumocytes isolated from the lizardPogona vitticeps

1999 ◽  
Vol 277 (6) ◽  
pp. R1705-R1711 ◽  
Author(s):  
Philip G. Wood ◽  
Olga V. Lopatko ◽  
Sandra Orgeig ◽  
Jonathan R. Codd ◽  
Christopher B. Daniels
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pulmonary Surfactant ◽  
Parasympathetic Nervous System ◽  
Work Of Breathing ◽  
Type Ii Cells ◽  
Type Ii ◽  
Type Ii Pneumocytes ◽  
Surfactant Secretion ◽  
Sympathetic Nervous

Pulmonary surfactant, a mixture consisting of lipids and proteins and secreted by type II cells, functions to reduce the surface tension of the fluid lining of the lung, and thereby decreases the work of breathing. In mammals, surfactant secretion appears to be influenced primarily by the sympathetic nervous system and changes in ventilatory pattern. The parasympathetic nervous system is not believed to affect surfactant secretion in mammals. Very little is known about the factors that control surfactant secretion in nonmammalian vertebrates. Here, a new methodology for the isolation and culture of type II pneumocytes from the lizard Pogona vitticeps is presented. We examined the effects of the major autonomic neurotransmitters, epinephrine (Epi) and ACh, on total phospholipid (PL), disaturated PL (DSP), and cholesterol (Chol) secretion. At 37°C, only Epi stimulated secretion of total PL and DSP from primary cultures of lizard type II cells, and secretion was blocked by the β-adrenoreceptor antagonist propranolol. Neither of the agonists affected Chol secretion. At 18°C, Epi and ACh both stimulated DSP and PL secretion but not Chol secretion. The secretion of surfactant Chol does not appear to be under autonomic control. It appears that the secretion of surfactant PL is predominantly controlled by the autonomic nervous system in lizards. The sympathetic nervous system may control surfactant secretion at high temperatures, whereas the parasympathetic nervous system may predominate at lower body temperatures, stimulating surfactant secretion without elevating metabolic rate.

scholarly journals Social instability and immunity in rhesus monkeys: the role of the sympathetic nervous system

2015 ◽  
Vol 370 (1669) ◽  
pp. 20140104 ◽  
Author(s):  
John P. Capitanio ◽  
Steven W. Cole
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Lymph Nodes ◽  
Rhesus Monkeys ◽  
Plasma Catecholamines ◽  
Social Conditions ◽  
Type I ◽  
Social Instability ◽  
Stable Conditions ◽  
Sympathetic Nervous

Social instability can adversely affect endocrine, immune and health outcomes, and recent evidence suggests that the sympathetic nervous system (SNS) might mediate these effects. We conducted two studies with adult male rhesus monkeys ( Macaca mulatta ) to understand how social conditions affect measures of SNS activity and immune function. In Experiment 1, animals were socialized in stable social conditions, then were switched to unstable (stressful) social conditions, then were returned to stable conditions. Analysis revealed quadratic effects for measures of behaviour, urinary metabolites of epinephrine and norepinephrine, and expression of immune response genes: as expected, social instability adversely impacted most measures, and the effects remediated upon re-imposition of stable conditions. Cortisol levels were unaffected. In Experiment 2, we used the sympathomimetic drug methamphetamine to challenge the SNS; animals also underwent socialization in stable or unstable groups. Surprisingly, while methamphetamine elevated plasma catecholamines, responses in lymph nodes tracked the social, and not the drug, condition: social instability upregulated the density of SNS fibres in lymph nodes and downregulated Type I interferon gene expression. Together, these results indicate that the SNS is extremely sensitive to social conditions; full understanding of the adverse effects of social instability on health should therefore incorporate measures of this health-relevant system.

scholarly journals The sympathetic nervous system stimulates anti-inflammatory B cells in collagen-type II-induced arthritis

2011 ◽  
Vol 71 (3) ◽  
pp. 432-439 ◽  
Author(s):  
Georg Pongratz ◽  
Madlen Melzer ◽  
Rainer H Straub
Keyword(s):  
Nervous System ◽  
B Cells ◽  
Sympathetic Nervous System ◽  
B Cell ◽  
Late Phase ◽  
Dependent Manner ◽  
Collagen Induced Arthritis ◽  
Sympathetic Nervous ◽  
Anti Inflammatory

BackgroundAs previously shown, the sympathetic nervous system (SNS) shows proinflammatory activity during initiation of arthritis but is anti-inflammatory in established collagen-induced arthritis (CIA). Interleukin 10 (IL-10)-producing B cells suppress arthritis and are a potential target of the SNS because (1) B cells express functional β2-adrenoceptors (β2ARs) and (2) IL-10, at least in monocytes/macrophages, is regulated in a cAMP/PKA/CREB-dependent manner.ObjectiveTo test the hypothesis that anti-inflammatory effects of the SNS in CIA are mediated by stimulating IL-10-producing anti-inflammatory B cells.MethodsCollagen-induced arthritis in DBA/1 mice, sympathectomy, adoptive B cell transfer, in vitro B cell culture, and assessment of B cell IL-10 production.Results and conclusionMice treated with B cells from SNS-intact mice showed less severe arthritis than mice treated with B cells from sympathectomised mice. This anti-inflammatory action of B cells from SNS-intact mice correlated with increased IL-10 produced by B cells, which was mediated by norepinephrine (NE), in a β2AR, PKA-dependent manner. However, an NE-mediated increase in IL-10 was seen only in B cells from immunised but not naive mice, explaining in part the anti-inflammatory properties of the SNS in the late phase of arthritis. Finally, animals treated with B cells isolated from immunised mice and activated in vitro in the presence of a β2AR stimulus showed a decrease in arthritis severity in comparison with controls, an approach that might be used for future cellular treatment strategies.

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