Long-term cardiopulmonary function after thoracic sympathectomy

These evaluations were performed again 1 year after the procedure to assess the long-term effects of sympathectomy.
Lung function tests revealed a significant decrease in forced expiratory volume in 1 second (FEV1) and forced expiratory flow between 25% and 75% of vital capacity (FEF25%–75%) in both groups (FEV1 of −6.3% and FEF25%–75% of −9.1% in the conventional thoracic sympathectomy group and FEV1 of −3.5% and FEF25%–75% of −12.3% in the simplified thoracic sympathectomy group). Dlco and heart rate at rest and maximal values after exercise were also significantly reduced in both groups (Dlco of −4.2%, Dlco corrected by alveolar volume of −6.1%, resting heart rate of −11.8 beats/min, and maximal heart rate of −9.5 beats/min in the conventional thoracic sympathectomy group and Dlco of −3.9%, Dlco corrected by alveolar volume of −5.2%, resting heart rate of −10.7 beats/min, and maximal heart rate of −17.6 beats/min in the simplified thoracic sympathectomy group). Airway resistance increased significantly in the group of patients undergoing conventional thoracic sympathectomy (+13%).
http://www.jtcvsonline.org/article/PIIS0022522309007569/abstract?rss=yes

TNF at a site of immunological injury may lead to chronic activation of innate immune cells and to chronic inflammatory responses

There is now good evidence to demonstrate that aberrations in tumour necrosis factor (TNF) production in vivo may be either pathogenic or protective and several plausible mechanisms may explain these contrasting activities. According to the classic pro-inflammatory scenario, failure to regulate the production of TNF at a site of immunological injury may lead to chronic activation of innate immune cells and to chronic inflammatory responses, which may consequently lead to organ specific inflammatory pathology and tissue damage.
http://www.ncbi.nlm.nih.gov/pubmed/10577971

dysregulation between the nervous and immune systems might contribute to disease development and progression

Data show that the nervous and immune systems communicate with one another to maintain immune homeostasis. Activated immune cells secrete cytokines that influence central nervous system activity, which in turn, activates output through the peripheral nervous system to regulate the level of immune cell activity and the subsequent magnitude of an immune response. In this review, we will focus our presentation and discussion on the findings that indicate a regulatory role for the peripheral sympathetic nervous system in modulating the level of cytokine and antibody produced during an immune response. Data will be discussed from studies involving the stimulation of the ß₂ adrenergic receptor expressed on CD4⁺ T cells and B cells by norepinephrine or selective agonists. We will also discuss how dysregulation of this line of communication between the nervous and immune systems might contribute to disease development and progression.
http://www.jleukbio.org/cgi/content/abstract/79/6/1093

Alterations in cytokine and antibody production following chemical sympathectomy

It is becoming clear that immune responses are subject to modulation by the sympathetic nervous system. We examined the effect of chemical sympathectomy (to ablate peripheral sympathetic nerve fibers) on cytokine and Ab production in two strains of mice that are known to differ in their response to a variety of pathogens and in the dominant types of cytokines produced. C57Bl/6J mice produce a strong cell- mediated response, characterized by production of IL-2 and IFN-gamma, whereas BALB/cJ have a dominant humoral response, with production of IL- 4 and IL-10. Animals were denervated by injection with 6- hydroxydopamine and immunized with keyhole limpet hemocyanin, and spleens were removed at various times after immunization. Denervation significantly increased the keyhole-limpet-hemocyanin-stimulated in vitro proliferation and IL-2 and IL-4 production by splenocytes from both strains.
http://www.jimmunol.org/cgi/content/abstract/155/10/4613

cytokines mediate and control immune and inflammatory responses

Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health.
http://www.ncbi.nlm.nih.gov/pubmed/16166805

Denervation resulted in increased production of tumor necrosis factor-α

by TA Callahan - 2002
linkinghub.elsevier.com/retrieve/pii/S0889159100906184

Tumor necrosis factor-a induces oligodendrocytes apoptosis

Tumor necrosis factor-a induces oligodendrocytes apoptosis, and is known to stimulate the hydrolysis of sphingomyelin to form the lipid mediator, ceramide.
http://www.springerlink.com/content/mu032lj427l85701/

Oligodendrocyte apoptosis and primary demyelination

We demonstrate that local production of TNF (tumor necrosis factor) by central nervous system glia potently and selectively induces oligodendrocyte apoptosis and myelin vacuolation in the context of an intact blood-brain barrier and absence of immune cell infiltration into the central nervous system parenchyma. Interestingly, primary demyelination then develops in a classical manner in the presence of large numbers of recruited phagocytic macrophages, possibly the result of concomitant pro-inflammatory effects of TNF in the central nervous system, and lesions progress into acute or chronic MS-type plaques with axonal damage, focal blood-brain barrier disruption, and considerable oligodendrocyte loss. Both the cytotoxic and inflammatory effects of TNF were abrogated in mice genetically deficient for the p55TNF receptor demonstrating a dominant role for p55TNF receptor-signaling pathways in TNF-mediated pathology.
http://www.ncbi.nlm.nih.gov/pubmed/9736029

Sympathectomy induces adrenergic excitability of cutaneous C-fiber nociceptors

1: J Neurophysiol. 1996 Jan;75(1):514-7.