Activation of NK Cells in Subjects Exposed to Mild Hyper- or Hypothermic Load

Lackovic, V; Borecký, L; Vigaŝ, M; Rovenský, Jozef

doi:10.1089/jir.1988.8.393

Cited by 31 publications

(15 citation statements)

References 15 publications

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“…Moderate cooling (in vivo studies) increases natural killer cell activity (11,34), white blood cell counts, (24) and monocytic expression of IL-6 and TNF-␣ (11) in human subjects. In vitro studies using human cell lines incubated at 32°C and 33°C showed increased IL-10 and decreased interferon gamma cytokine gene expression in peripheral blood cultures (49), decreased production of IL-10 in peripheral mononuclear blood cells (41), and prolonged activation of nuclear factor B and increased proinflammatory cytokine gene expression in LPS- Fig.…”

Section: Discussionmentioning

confidence: 99%

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

Ganta

Helwig²,

Blecha³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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. Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system. Am J Physiol Regul Integr Comp Physiol 291: R558 -R565, 2006. First published February 9, 2006 doi:10.1152/ajpregu.00846.2005.-Splenic nerve denervation abrogates enhanced splenic cytokine gene expression responses to acute heating, demonstrating that hyperthermia-induced activation of splenic sympathetic nerve discharge (SND) increases splenic cytokine gene expression. Hypothermia alters SND responses; however, the role of the sympathetic nervous system in mediating splenic cytokine gene expression responses to hypothermia is not known. The purpose of the present study was to determine the effect of hypothermia on the relationship between the sympathetic nervous system and splenic cytokine gene expression in anesthetized F344 rats. Gene expression analysis was performed using a microarray containing 112 genes, representing inflammatory cytokines, chemokines, cytokine/chemokine receptors and housekeeping genes. A subset of differentially expressed genes was verified by real-time RT-PCR analysis. Splenic SND was decreased significantly during cooling (core temperature decreased from 38 to 30°C) in splenicintact rats but remained unchanged in sham-cooled splenic-intact rats (core temperature maintained at 38°C). Hypothermia upregulated the transcripts of several genes, including, chemokine ligands CCL2, CXCL2, CXCL10, and CCL20, and interleukins IL-1␣, IL-1␤, and IL-6. Gene expression responses to hypothermia were similar for the majority of cytokine genes in splenic-intact and splenic-denervated rats. These results suggest that hypothermia-enhanced splenic cytokine gene expression is independent of splenic SND.hypothermia; splenic cytokine gene expression; splenic sympathetic nerve discharge EVIDENCE FROM THE DISCIPLINES of neuroscience and immunology demonstrate bidirectional communication pathways between the sympathetic nervous system and the immune system (2, 3, 13, 38). Sympathetic innervation to the spleen provides a connection between central sympathetic neural circuits and immunocompetent cells in the spleen (1,6,9,16,17). For example, chemical sympathectomy alters splenic T and B cell proliferation and natural killer cell activity (36 -40, 45) and diminishes splenic production of immunoglobulin M (31). Results of our recent studies demonstrate that in rats with intact splenic nerves, whole body hyperthermia (19) and central ANG II infusion (20) increase splenic sympathetic nerve discharge (SND) and the expression of selective splenic cytokine genes. Splenic cytokine gene expression responses to whole body hyperthermia and central ANG II infusion are significantly reduced in splenic nerve-denervated compared with splenic nerve-intact rats (19,20), suggesting that activation of splenic SND can enhance splenic cytokine gene expression.Hypothermia, a common side effect of extreme cold environments, anesthesia, and serious traumatic injuries, alters the sympathetic nervous system and immune system regula...

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Section: Discussionmentioning

confidence: 99%

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

Ganta

Helwig²,

Blecha³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Icv injection of losartan decreases levels of resting renal SND in rats with chronic heart failure (11), and chronic central AT 1 receptor blockade normalizes the enhanced sympathoexcitation, reduced sympathoinhibition, and desensitized baroreflex responses observed in congestive heart failure rats after myocardial infarction (56). Congestive heart failure patients exhibit clinical features that are observed in chronic inflammatory conditions (10,34,50). For example, plasma levels of proinflammatory cytokines, notably IL-6 and TNF-alpha, are elevated in congestive heart failure patients and serum levels of IL-10, a potent anti-inflammatory cytokine, are reduced (10,34,50).…”

Section: Real-time Rt-pcr Analysis Of Splenic Gene Expression Responsmentioning

confidence: 99%

“…Congestive heart failure patients exhibit clinical features that are observed in chronic inflammatory conditions (10,34,50). For example, plasma levels of proinflammatory cytokines, notably IL-6 and TNF-alpha, are elevated in congestive heart failure patients and serum levels of IL-10, a potent anti-inflammatory cytokine, are reduced (10,34,50).…”

Section: Real-time Rt-pcr Analysis Of Splenic Gene Expression Responsmentioning

confidence: 99%

“…A role for the sympathetic nervous system in immune regulation is supported by the innervation of lymphoid organs (including the spleen) by sympathetic nerves (15)(16)(17)(18)(19) and the presence of adrenergic receptors on immune cells (8,34,39,42,48). A role for the immune system in sympathetic nerve regulation is supported by the increased rate of norepinephrine release and turnover in spleen and bone marrow following activation of antigenspecific T cells and B cells by a soluble protein antigen (35) and changes in the level of SND produced by administration of IL-1β antibody (43) and IL-1β (25,56).…”

Section: Introductionmentioning

confidence: 99%

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#45 Central activation of sympathetic neural circuits alters splenic cytokine gene expression

Ganta

Lü

Helwig

et al. 2005

Brain, Behavior, and Immunity

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Important bidirectional interactions exist between the central nervous system and the immune system. Neural-immune interactions provide a regulatory system in the body and disturbances in these interactions may lead to disease. Although the sympathetic nervous system is thought to play a key role in mediating neural-immune interactions, central neural mechanisms mediating sympathetic-immune interactions and the effect of centrally-induced alterations in sympathetic nerve discharge on immune function is not known. We tested the hypothesis that central activation of sympathetic neural circuits alters splenic cytokine gene expression. In a separate study, we tested the hypothesis that hypothermia-induced changes in visceral sympathetic nerve discharge (SND) would be attenuated in middle-aged and aged compared with young rats. Previous studies have demonstrated that skin sympathoexcitatory responses to skin cooling are attenuated in aged compared with young subjects, suggesting that advancing age influences sympathetic nerve responsiveness to cooling. The effect of age on sympathetic nerves innervating other targets organs during acute cooling remains unknown. Central activation of splenic SND was produced using three different experimental interventions: increased core body temperature produced by acute heating, intracerebroventricular injection of angiotensin II (ANG II), and decreased core body temperature produced by acute cooling. Changes in gene expression profiles were analyzed using inflammatory cytokine-specific gene-array and further validated using real-time RT-PCR analysis. The following observations were made. 1) Splenic SND increased in response to each experimental intervention except in acute cooled young rats where there was a decrease in splenic SND. 2) Splenic cytokine gene expression of pro-inflammatory cytokines (e.g., IL-1β, IL-6, IL-2) and chemokines (GRO1, CXCL2, CCCL2 and, CXCL10) was increased in response to each experimental intervention. 3) Expression of splenic cytokine genes was reduced after splenic-denervation except in acute cooled rats. 4) Progressive hypothermia reduced splenic, renal, and adrenal SND in rats and was generally attenuated in middle-aged and aged rats. These results demonstrate the functional significance of changes in sympathetic nerve activity on splenic immune cell activation and the effect of age on SND responses to core body ABSTRACTImportant bidirectional interactions exist between the central nervous system and the immune system. Neural-immune interactions provide a regulatory system in the body and disturbances in these interactions may lead to disease. Although the sympathetic nervous system is thought to play a key role in mediating neural-immune interactions, central neural mechanisms mediating sympathetic-immune interactions and the effect of centrally-induced alterations in sympathetic nerve discharge on immune function is not known. We tested the hypothesis that central activation of sympathetic neural circuits alters splenic cytokine gene expr...

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“…Furthermore, a brief bout (30 min) of cold (4°C) air exposure increases NK cell activity (60). We thus hypothesized that exposure to cold air (5°C) for 2 h would have immunostimulating effects and that pre-treatment with exercise or passive heating would have algebraically additive effects on this response.…”

Section: Immersion Of Healthy Young Men In Cold (14°c) Water Induces mentioning

confidence: 99%

Thermoregulatory and Immune Responses During Cold Exposure: Effects of Repeated Cold Exposure and Acute Exercise

Castellani¹,

Young²,

Sawka³

et al. 2000

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Activation of NK Cells in Subjects Exposed to Mild Hyper- or Hypothermic Load

Cited by 31 publications

References 15 publications

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

Hypothermia-enhanced splenic cytokine gene expression is independent of the sympathetic nervous system

#45 Central activation of sympathetic neural circuits alters splenic cytokine gene expression

Thermoregulatory and Immune Responses During Cold Exposure: Effects of Repeated Cold Exposure and Acute Exercise

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