Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proinflammatory cytokines have been identified in herniated intervertebral discs in humans, and such cytokines have experimentally been demonstrated to be important in the pathophysiological mechanisms of disc herniation. Cerebrospinal fluid (CSF) and serum concentrations of interleukin (IL)-1beta IL-6, IL-8, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha were investigated using the enzyme-linked immunosorbent assay (ELISA) technique in 39 patients with lumbar disc herniation and sciatica. Pain duration and pain intensity (visual analogue scale, VAS) were recorded at inclusion, and a clinical examination was performed evaluating neurological findings. The extent of disc herniation (protrusion or extrusion/sequestration) was evaluated perioperatively. Normal concentrations of IL-1beta, IL-6, IFN-gamma and TNF-alpha were present in CSF and serum in almost all patients with lumbar disc herniation. The concentrations of IL-8 in CSF were increased in 12 out of 39 patients, and these increased levels of IL-8 correlated to a short duration of pain and to more pronounced herniation (extrusion or sequestration). No relationship between IL-8 concentrations in CSF and pain intensity, positive neurological findings or a positive straight leg-raising (SLR) test was found. The observation of increased concentrations of IL-8 in CSF in patients with a short duration of symptoms supports the concept of the initial involvement of inflammatory mechanisms after a disc herniation. The finding that most of the patients with increased concentrations of IL-8 in CSF had an extrusion or a sequestration may suggest that the increase in IL-8 is related to mechanical nerve root compression, but may also indicate a biochemical effect exerted by the herniated disc on the surrounding tissue. Further studies on the potential role of IL-8 as a biomarker for disc herniation are warranted.
 ...
PMID:Proinflammatory cytokines in cerebrospinal fluid and serum in patients with disc herniation and sciatica. 1193 Oct 66

The sympathetic system (SNS) is considered to be a major component of the neurogenic contribution to inflammation and hyperalgesia. We have investigated the role of the SNS in the local inflammatory pain induced by intraplantar (i.pl) injections of bacterial endotoxin (ET). Treatment of rats with an alpha-adrenoceptor antagonist (phentolamine, 0.25-1 mg/kg, i.p.), a beta-adrenoceptor antagonist (propranolol, 1-10 mg/kg, p.o.) or a sympathetic neuron-blocking agent (guanethedine, 30 mg/kg, s.c.) resulted in a dose-dependent reduction of the thermal hyperalgesia induced by ET. Mechanical hyperalgesia, however, was less sensitive to inhibition by propranolol and guanethedine but significantly inhibited by phentolamine. ET injection produced significant upregulation of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, and nerve growth factor (NGF). Treatment with any one of the three sympatholytics abolished the upregulation of NGF and IL-6, while phentolamine and guanethedine also reversed the upregulation of TNF-alpha. IL-1 beta was resistant to all of the sympatholytic treatments. We conclude that the SNS can contribute to the local inflammation and hyperalgesia following injection of ET. The resistance to sympatholytics shown by IL-1 beta, known to play a key role in the inflammatory cascade, suggests that ET can initiate inflammation and hyperalgesia independently of peripheral and central sympathetic mechanisms.
 ...
PMID:The role of the sympathetic efferents in endotoxin-induced localized inflammatory hyperalgesia and cytokine upregulation. 1201 13

Acupuncture has become quite familiar to many Koreans not only for pain, but also for many other health problems, both in acute and chronic conditions. Actually, acupuncture is a therapeutic technique that is part of a larger system of traditional oriental medicine. There are several styles of acupuncture. We investigated the regulatory effects of cytokine production in peripheral blood of asthma patients (AP) by SOOJI CHIM (Koryo Hand Acupuncture Therapy, KHT). Clinical signs of asthma disappeared markedly by KHT. The mean interleukin (IL)-2 and IL-6 plasma levels were lower in the AP group than in the normal group, whereas the mean interferon (IFN)-gamma, IL-4, and tumor necrosis factor (TNF)-alpha levels were higher in the AP group. Plasma IFN-gamma and IL-2 levels derived from T helper (Th)1 cells and IL-4 levels derived from Th2 cells were elevated in the AP group by KHT. Especially, plasma IL-6 levels derived from Th2 cells were elevated significantly in the AP group by KHT. Reduced plasma levels of TNF-alpha were observed in the AP group by KHT. Plasma IgE levels were also measured but there were no significant differences from each other. During the KHT, there were no other adverse effects. These results indicate that KHT has a good asthma treatment effect, and that its action may be due to the regulation of cytokine production.
 ...
PMID:Regulatory effect of cytokine production in asthma patients by SOOJI CHIM (Koryo Hand Acupuncture Therapy). 1206 52

When tissue is destroyed, pain arises. Tissue destruction as well as wound healing are associated with an inflammatory reaction. This leads to activation of nociceptors ("pain receptors") which can cross-communicate with the inflammatory infiltrate. The following review will concentrate on pain-exaggerating (hyperalgesic) and pain-ameliorating (analgesic) mediators which arise from immune cells or the circulation during the inflammation. In the early stages of inflammation endogenous hyperalgesic mediators are produced, including the proinflammatory cytokines IL-1, IL-6 and TNF-alpha, nerve growth factor as well as bradykinin and prostaglandins. Simultaneously, analgesic mechanisms are activated. Opioid peptides such as endorphins, enkephalins and dynorphins are produced by immune cells and can be released locally in the inflamed tissue on stimulation with IL-1 or corticotropin releasing factor. Analgesia is elicited by binding of the opioid peptides to receptors on peripheral sensory neurons. During the course of an inflammatory process, peripheral opioid-mediated analgesia increases. In parallel, antiinflammatory cytokines such as IL-4, IL-10, IL-13 and IL-1ra are produced and reduce hyperalgesic effects of the proinflammatory cytokines initially produced. Inflammatory pain, therefore, is the result of an interplay between hyperalgesic and analgesic mediators. Drugs such as immunosuppressants influencing this interplay may also impair endogenous hyperalgesic and analgesic mechanisms.
 ...
PMID:[Pain and the immune system: friend or foe?]. 1212 5

Feline osteoclastic resorptive lesions (FORL) of the teeth are common in cats, and lead to pain, destruction of the periodontal ligament, and tooth loss. The expression of interleukin (IL)-1 beta and IL-6 mRNA was higher in teeth with FORL than in normal teeth (P<0.01 and P<0.001, respectively), but no such differences were found between pathological and normal gingival tissue samples. There were no differences between teeth affected with FORL and normal teeth in respect of the expression of receptor activator of NF kappa B ligand (RANKL) mRNA or osteoprotegerin (OPG) mRNA. However, OPG mRNA expression was higher in gingival tissue associated with teeth affected with FORL than in normal gingival tissue (P<0.05), whereas the reverse was true of RANKL mRNA expression (P<0.05). OPG mRNA expression was significantly higher in teeth than in femoral and alveolar bone (P<0.001). RANKL and OPG mRNAs were detected in all tissues examined. The data suggest that the elevated expression of IL-l beta and IL-6 mRNA plays a role in the mediation of osteoclast activity in advanced FORL. In contrast, OPG and RANKL do not appear to regulate osteoclasts in advanced disease. The results also suggest that OPG and RANKL mRNA play a role in mediating inflammatory responses in gingival cells, and that OPG has an inhibiting effect on tooth resorption.
 ...
PMID:Cytokine expression in feline osteoclastic resorptive lesions. 1235 28

Hypersensitivity resulting from nerve injury or morphine tolerance/hyperalgesia is predicted to involve similar cellular and molecular mechanisms. One expected but incompletely explored mechanism is the activation of central neuroimmune responses associated with these conditions. To begin to address this, we undertook three separate studies: First, we determined the acute antinociceptive action of morphine, the rate of development of opioid tolerance, and withdrawal-induced hyperalgesia/allodynia in nerve-injured and sham-operated rats using noxious (thermal and mechanical) and non-noxious (mechanical allodynia) behavioral paradigms. Second, we investigated the impact of chronic morphine treatment on spinal glial activation and cytokine expression after L5 spinal nerve transection or sham surgery. Third, we examined the consequences of spinal administration of cytokine inhibitors on the development of morphine tolerance and morphine withdrawal-induced hyperalgesia and allodynia. Results demonstrated that after nerve injury, the antinociceptive effect of acute morphine was significantly decreased, and the rate of development of tolerance and opioid withdrawal-induced hyperalgesia/allodynia was significantly enhanced compared with that after sham surgery. Chronic administration of morphine to sham-operated rats activated spinal glia and upregulated proinflammatory cytokines [interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha]. This neuroimmune activation was further enhanced in nerve-injured rats after chronic morphine treatment. Spinal inhibition of proinflammatory cytokines restored acute morphine antinociception in nerve-injured rats and also significantly reversed the development of morphine tolerance and withdrawal-induced hyperalgesia and allodynia in nerve-injured or sham-operated rats. Targeting central cytokine production and glial activation may improve the effectiveness of morphine and reduce the incidence of morphine withdrawal-induced hyperalgesia and allodynia in neuropathic pain conditions.
 ...
PMID:The role of spinal neuroimmune activation in morphine tolerance/hyperalgesia in neuropathic and sham-operated rats. 1242 55

The purpose of this study was to evaluate the effects of laparoscopic surgery on the symptoms associated with ovarian endometrioma. We also examined serum IL-6 concentrations in patients with endometrioma. Ninety-two patients who underwent laparoscopic surgery for ovarian endometrioma were enrolled in this study. The mean duration of follow-up was 27.6 months. Transvaginal ultrasound examinations revealed a recurrence of endometrioma in 13% of the cases. We evaluated the severity of dysmenorrhea using a 0-3-point verbal rating scale, and found that the dysmenorrhea score was statistically improved after the operation. Follicular growth was preserved in 94%, and the pregnancy rate was 43%. We measured serum IL-6 concentrations in 14 patients with ovarian endometrioma and 4 patients with benign gynecologic disease without endometriosis. IL-6 was significantly higher in patients with endometrioma than in those without endometriosis at the time of diagnosis. The mean serum IL-6 concentration significantly decreased after the operation. In conclusion, laparoscopic surgery is effective for alleviating pain and preserving fertility in patients with endometrioma. Measurements of serum IL-6 concentrations may be useful for the management of endometrioma.
 ...
PMID:Laparoscopic surgery for the management of ovarian endometrioma. 1244 57

Mastalgia is a common condition that is thought to be hormonally related, but the mechanisms of pain causation are unknown. Inflammatory cytokines are implicated in pain modulation, but have not been studied with regard to mastalgia. We compared the relationship of mastalgia to the expression of the cytokines interleukin (IL)-6, IL-1beta, and tumor necrosis factor (TNF)-alpha and the degree of tissue infiltration with inflammatory cells in breast tissue from 29 premenopausal women with breast pain and 29 age-matched pain-free controls. Paraffin sections from breast biopsy samples were scored for the presence of inflammatory infiltrate and were evaluated for the expression of IL-6, IL-1beta, and TNF-alpha using standard immunohistochemical procedures. TNF-alpha and IL-6 expression displayed a trend toward slightly lower values in patients with pain (median TNF-alpha score, 3 versus 5; median IL-6 score, 3 versus 4). In the luteal phase, patients with mastalgia showed a trend toward lower expression of IL-6 (p = 0.4) in comparison to those without pain. A similar trend was also seen with TNF-alpha expression (p = 0.4). IL-1beta expression was extremely scant in the first 30 samples and was not investigated further. The degree of inflammatory infiltrate in the tissue was unrelated to the presence of breast pain. These data suggest that the three cytokines tested in this study do not play a significant role in the causation of mastalgia and lend weight to the previous finding that there are no identifiable histologic correlates of this troubling condition. Further investigation of the role of cytokines in breast pain is warranted, especially in view of the possible association between mastalgia and breast cancer risk.
 ...
PMID:Expression of interleukin-6 and tumor necrosis factor alpha and histopathologic findings in painful and nonpainful breast tissue. 1260 81

Recent advancements in the pain field have identified a central nervous system (CNS) neuroimmune response that may act as the driving force for neuronal hypersensitivity, the pathological correlate to chronic pain following peripheral nerve injury. Neuroimmune activation involves the activation of nonneuronal cells such as endothelial and glial cells, which when stimulated leads to enhanced production of a host of inflammatory mediators, such as cytokines. The central production of proinflammatory cytokines, such as interleukin-1beta (IL-1beta), IL-6 and tumor necrosis factor have been found to play a key role in the propagation of persistent pain states. In addition, chemotactic cytokines, chemokines, have also been recently identified in the CNS neuroimmune cascade that ensues after injury to a peripheral nerve. The extravasation of leukocytes from the blood to the site of perceived injury is defined as the neuroinflammatory aspect of this cascade. Chemokines directly control this leukocyte transmigration process. They are synthesized at the site of injury and establish a concentration gradient through which immune cells migrate. Recent studies have demonstrated leukocyte trafficking into the CNS following peripheral nerve or lumbar nerve root injury. With the use of selective cytokine inhibitors and neutralizing antibodies, tactile and thermal hypersensitivity is attenuated in animal models of neuropathy. A further understanding of the role of nonneuronal cells, the physiological mechanisms of CNS cytokines and chemokines, and their relevance to neuro- immune activation and neuroinflammatory processes may lead to the development of novel pharmacological agents for the treatment and prevention of chronic pain. (c) 2002 Prous Science. All rights reserved.
 ...
PMID:The Role of Cytokines in the Initiation and Maintenance of Chronic Pain. 1267 47

Proinflammatory cytokines are supposed to play a major role in the pathophysiology of vasculitis and in the development of neuropathic pain. Here we studied the cytokine expression in sural nerve biopsy specimens from patients with vasculitic and other inflammatory and non-inflammatory neuropathies, and investigated whether an increased cytokine expression was correlated with the presence of neuropathic pain. We used immunohistochemistry including double labeling and morphometry to localize and quantify the expression of interleukin-1 beta (IL-1beta), IL-6, and tumor necrosis factor-alpha (TNF) in sural nerve biopsy samples of 41 patients with vasculitic neuropathy (VANP), chronic inflammatory demyelinating neuropathy (CIDP), non-inflammatory chronic axonal neuropathy (CANP), and 3 controls. Overall cytokine immunoreactivity was highest in VANP, less strong in CIDP and lowest in CANP. Cytokine immunoreactivity was directly correlated with the degree of axonal degeneration, endoneurial macrophages and epineurial T cells. In VANP and CANP, a higher cytokine content was associated with neuropathic pain.
 ...
PMID:Cytokines in sural nerve biopsies from inflammatory and non-inflammatory neuropathies. 1273 66


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>