Brain, behavior, and immunity
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Brain Behav. Immun. · Jul 2005
Comparative StudySocial stress and the regulation of tumor necrosis factor-alpha secretion.
Social disruption (SDR), a murine model of social stress, altered the phenotype and function of spleen immune cells. Previous reports indicated that following SDR spleens contained higher numbers of CD11b+ monocytes, and these cells were less sensitive to the inhibitory effects of glucocorticoids on cell viability. Additionally, lipopolysaccharide (LPS)-stimulated splenocytes from SDR mice secreted higher levels of the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 compared to splenocytes from controls. ⋯ We report that SDR increased TNFalpha secretion from an enriched fraction of CD11b+ monocytes stimulated with LPS. Additionally, SDR altered the kinetics of TNFalpha release from LPS-stimulated splenocytes and induced minor changes in the suppressive effects of corticosterone and norepinephrine on LPS-induced TNFalpha secretion. These results are in agreement with the notion that complex interactions mediate the response to social stress.
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Brain Behav. Immun. · Jul 2005
Clinical Trial Controlled Clinical TrialCortical correlates of false expectations during pain intensity judgments--a possible manifestation of placebo/nocebo cognitions.
We investigated the effects of expectation on intensity ratings and somatosensory evoked magnetic fields and electrical potentials following painful infrared laser stimuli in six healthy subjects. The stimulus series contained trials preceded by different auditory cues which either contained valid, invalid or no information about the upcoming laser intensity. High and low intensities occurred equally probable across cue types. ⋯ Its amplitude also varied with stimulus intensity, but failed to show any cue validity effects. This result suggests a priming of early cortical nociceptive sensitivity by cues signaling pain severity. A possible contribution of the SII cortex to the manifestation of nocebo/placebo cognitions is discussed.
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Brain Behav. Immun. · Mar 2005
ReviewImmune-to-brain communication dynamically modulates pain: physiological and pathological consequences.
This review examines recently recognized roles of immunological processes in pain modulation and explores the potential implications of these immunologically derived phenomena for human chronic pain control. The focus is an examination of how activation of immune-like glial cells within the spinal cord can amplify pain by modulating the excitability of spinal neurons. Such glially driven enhancement of pain can be physiological, as occurs in response to peripheral infection or inflammation. ⋯ Here, immune- and trauma-induced alterations in peripheral nerve function lead to the release of substances within the spinal cord that trigger the activation of glia. Evidence is reviewed that such pathologically driven glial activation is associated with enhanced pain states of diverse etiologies and that such pain facilitation is driven by glial release of proinflammatory cytokines and other neuroexcitatory substances. This recently recognized role of spinal cord glia and glially derived proinflammatory cytokines as powerful modulators of pain is exciting as it may provide novel approaches for controlling human chronic pain states that are poorly controlled by currently available therapies.
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Brain Behav. Immun. · Mar 2005
Marginating pulmonary-NK activity and resistance to experimental tumor metastasis: suppression by surgery and the prophylactic use of a beta-adrenergic antagonist and a prostaglandin synthesis inhibitor.
Surgery is imperative for cancer treatment, but was suggested to suppress immunity and facilitate metastasis. Here we study the involvement of catecholamines and prostaglandins (PG) in such outcomes, and the role played by marginating-pulmonary (MP)-NK cells in controlling MADB106 metastasis. Non-operated and laparotomized F344 rats were injected postoperatively with a PG synthesis inhibitor (indomethacin, 4 mg/kg i.p.), a beta-blocker (nadolol, 0.6 mg/kg s.c.), both drugs, or vehicle. ⋯ Alterations in the numbers of NK cells were partly associated with alterations in total MP-NK activity, but not with circulating-NK activity. Last, administrating nai ve rats with physiologically relevant doses of a beta-adrenergic agonist (metaproterenol), and/or with PGE2, additively and independently of each other promoted MADB106 metastasis, simulating the effects of surgery. These findings point at potential prophylactic measures in cancer patients undergoing surgery, and suggest a role for MP-NK cells in resisting metastasis of apparently insensitive tumors.
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Brain Behav. Immun. · Jul 2004
Clinical Trial Controlled Clinical TrialPain, psychological variables, sleep quality, and natural killer cell activity in midlife women with and without fibromyalgia.
In women with fibromyalgia (FM), central nervous system (CNS) dysfunction in pain, mood, and sleep processes could be associated with changes in immune system indicators. The primary purpose of this study was to compare pain, psychological variables, subjective and objective sleep quality, lymphocyte phenotypes and activation markers, and natural killer activity (NKA) in midlife women with and without FM. A secondary purpose was to explore relationships among these variables in a step-wise regression. ⋯ NKA was not statistically significantly lower in the women with FM compared to controls. In a multiple regression of age, tender point threshold, depression, psychological distress, and sleep efficiency, only the effect of group was significant (F = 5.479, p <.03) on NKA. In conclusion, we found little evidence to support the hypothesis that pain, mood, and sleep symptoms are associated with changes in the enumeration of peripheral lymphocytes or function in FM.