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We assayed IL-6 in 105 cerebrospinal fluid (CSF) samples from patients with ALS, MS, HTLV-1 associated myelopathy (HAM), and controls. There was considerable overlap in IL-6 levels in all patient groups. The mean IL-6 in 27 patients with ALS was significantly higher than in 21 patients in the other neurological disease (OND) group (P=0.0075). There were no significant differences in MS or HAM and the OND control group. Overall, CSF IL-6 correlated with protein concentration but not with percentage IgG or IgG-albumin index. Patients with CSF oligoclonal bands were no more likely to have detectable IL-6 than patients without oligoclonal bands. Similarly, IL-6 did not correlate with clinical disease activity in MS when subgroups of patients were compared or when an individual patient was followed over time. The elevated IL-6 in ALS may reflect an ongoing humoral immune response, or IL-6 may be non-specifically expressed in these patients as a putative neurotrophic factor in response to nerve cell degeneration.
Eye tissues respond to physiological and pathophysiological stimuli by the activation of phospholipases and the consequent release from membrane phospholipids of biologically active metabolites. These rapid events have profound effects on long-term ocular physiology. Activation of phospholipase A2 is the first step in the synthesis of two important classes of lipid second messengers, the eicosanoids and platelet-activating factor (PAF). PAF accumulates in the cornea in response to injury. It has been shown to stimulate metalloproteinase gene expression in the corneal epithelium, and is, thus, implicated in the extracellular matrix remodeling that accompanies wound healing and ulceration. PAF antagonists confer protection in animal models of acute and chronic anterior segment inflammation, and block the PAF-enhanced glutamate release from retina. The latter effect suggests a role for PAF in glaucomatous neuronal damage. The eicosanoids, in particular the prostaglandins, have long been implicated in the pathophysiology of ocular inflammation and there is pharmacological evidence for their role in the regulation of intraocular pressure. The induction by PAF of the inducible prostaglandin synthase in neurons and in the corneal epithelium provides a link between the actions of these two lipid second messengers. There may be thresholds of lipid second messenger concentrations which govern their activities as physiological, defensive, or harmful.
Linomide (quinoline-3-carboxamide) is a synthetic immunomodulator that suppresses several experimental autoimmune diseases. Here we report the effects of Linomide on experimental autoimmune encephalomyelitis (EAE), a CD4+ T cell-mediated animal model of multiple sclerosis (MS). EAE induced in Lewis rats by inoculation with homogenized guinea pig spinal cord and Freund's complete adjuvant was strongly suppressed by Linomide administered daily subcutaneously from the day of inoculation. Linomide dose-dependently delayed the interval between immunization and onset of clinical EAE, and reduced severity of EAE symptoms. These clinical effects were associated with dose-dependent down-modulation of myelin antigens-induced T cell responses and by suppression of the proinflammatory cytokines IFN-gamma and TNF-alpha, and upregulation IL-4, IL-10 and TGF-beta as evaluated by in situ hybridization for mRNA expression in spleen mononuclear cells and spinal cord sections. These findings suggest that Linomide could be useful in certain T cell dependent autoimmune diseases.
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To investigate morphological changes occurring during cutaneous photoageing, a correlation between the number of infiltrating cells in the dermis and the degree of collagen damage was examined using sections from clinically normal chronically sun-exposed and sun-protected skin of Japanese female subjects. Haematoxylin and eosin-stained sections from 134 sun-exposed (subjects aged 3-82 years) and 73 sun-protected (subjects aged 1-86 years) areas demonstrated a predominant lymphoid cell and to a lesser extent histiocyte infiltration. The mean +/- SD number of lymphoid cells and histiocytes in the sun-exposed skin sections (427.0+/-192.2 and 147.8+/-83.3 cells/mm2, respectively) was significantly higher than in the sun-protected skin sections (292.6+/-98.3 and 125.9+/-59.0 cells/mm2, respectively) (P < 0.001 and P < 0.05, respectively), and the number of lymphoid cells in the sun-exposed skin sections increased significantly with age up to 50 years (r = 0.400, P < 0.001). Sun-exposed skin sections with severe collagen degeneration had a significantly higher number of lymphoid cells than those with slightly degenerated collagen (mean 626.3 vs. 482.4 cells/mm2, P < 0.01). The mean count of mast cells in sun-exposed skin was 202.0 cells/mm2; this did not vary with the age of the subjects or the level of collagen damage. Immunohistochemical studies using 24 frozen sections identified most of the lymphoid cells infiltrating sun-exposed skin as memory T lymphocytes (CD3+, CD4+ and CD45RO+). The number of cells which displayed immunoreactivity to matrix metalloproteinase (MMP)-1 in the sun-exposed skin sections was significantly higher than in the sun-protected skin sections (mean 170.2 vs. 113.6 cells/mm2, P < 0.05). Among these cells were observed CD3 and MMP-1 double-stained T lymphocytes, and T lymphocytes contacting MMP-1-positive cells. These morphological observations suggest that T lymphocytes infiltrating photodamaged skin may play a part in the degeneration and reduction of collagen through MMP-1 activity.
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OBJECTIVE: To study the relationship between reported chronic pain and the level of serum urate (SU) among women with various diagnoses of the musculoskeletal system. METHODS: Consecutive female patients (aged 20-70 years, n = 124), at rheumatology and rehabilitation practices, with chronic musculoskeletal pain of different origins were followed for 1 year after an initial survey of pain, lifestyle, quality of life, and disability. Repeated blood samples (including urate, creatinine, cholesterol, and glucose) were analysed. Multiple regression analysis was performed to explain initial variations in SU level in relation to pain and confounding factors. RESULTS: The level of SU was increased among individuals with widespread pain (>5 locations) independent of underlying diagnoses compared to those with fewer pain sites (270.5 vs. 241.2 micromol/L). Serum creatinine, body mass index (BMI), the number of pain locations, and sleep disturbances independently contributed to the SU level and explained 43% of the variation in SU. Individual variation in SU during 4 months was low. CONCLUSIONS: Epidemiological data on the relationship between the extent of body pain and SU were confirmed in a clinical setting. Besides known factors such as impaired renal function and obesity, widespread pain and sleep disturbances were related to an increase in SU. Medication and alcohol intake could not explain the findings. Longitudinal studies are necessary to elucidate whether the level of SU has any implications for the prognosis of chronic pain.
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Tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, -8 and-10 and soluble TNF receptor II (sTNFR II) levels were measured at baseline, and after antifungal therapy for 2 weeks and 3 months, in plasma from 75 human immunodeficiency virus (HIV)-positive and 14 HIV-negative patients with cryptococcosis, and in plasma from 14 HIV-positive controls. At baseline, TNF-alpha, IL-6 and sTNFR II levels, and cryptococcal antigen titres, were increased in patients with fungaemia compared to controls (p < 0.02). The mediator levels were not influenced by the severity of the disease or subsequent death, but sTNFR II and IL-10 levels were reduced, together with virus load, in patients receiving anti-retroviral agents (p < 0.01). During antifungal therapy, sTNFR II levels decreased (p 0.003) in parallel with the virus load and with an increase in CD4 T-cell numbers.