Reproductive hormones and interleukin-6 in serious leisure male athletes

Lifestyles associated with different types and intensities of exercise result in improved health including positive changes in chronic low-grade inflammatory biomarkers. Alternatively, some forms of exercise adversely affect reproductive health of men, including changes in circulating reproductive hormones. To explore the associations between exercise intensity and circulating levels of reproductive hormones, and inflammatory analytes in serious leisure athletes (triathletes and cyclists) and recreational athletes. Male athletes 18-60?years old, 16 triathletes, 46 cyclists and 45 recreational athletes, were recruited to provide plasma for the measurement of total testosterone, estradiol, follicular stimulating hormone, luteinizing hormone (LH), sex hormone-binding globulin (SHBG), cortisol, interleukin-6 (IL-6), and interleukin-1β (IL-1β) levels, and calculation of free androgen index (FAI) and the estradiol:SHBG ratio (ESR). Plasma estradiol concentrations were more than two times higher in cyclists than in triathletes and recreational athletes (p?相似文献   

Plasma eosinophil cationic protein, interleukin-5, and ECP/Eo count ratio in patients with various eosinophilic diseases

Hypereosinophilia is associated with clonal disorders, reactive conditions, and rarely with idiopathic hypereosinophilic syndrome (IHES). We investigated whether measurement of eosinophilic activity using the plasma eosinophil cationic protein (ECP) level, interleukin-5 (IL-5) level, and the ratio of eosinophilic cationic protein/eosinophil count (ECP/Eo) could improve the early differentiation among various eosinophilic diseases: IHES (n = 9), clonal disorder (n = 35), reactive eosinophilia with malignancy (n = 30), and reactive eosinophilia with inflammation (n = 46). The 120 eosinophilic patients had higher plasma ECP and IL-5 levels than the non-eosinophilic control group (p <0.05). The 9 patients with IHES had significantly higher plasma ECP and IL-5 levels than patients with other eosinophilic diseases (p <0.05). The plasma levels of ECP and the ECP/Eo ratio were higher in patients with non-haematologic malignancy than in those with other reactive eosinophilias (p <0.05). This study shows that levels of plasma ECP, IL-5, and ECP/Eo ratio may assist in the clinical differentiation of various eosinophilic diseases.     

Gammadelta T cells and interleukin-6 levels could provide information regarding the progression of human renal allograft

We have determined the percentage of alphabeta and gammadelta T cells by flow cytometry as well as serum interleukin-6 (IL-6) and soluble interleukin-6 receptor (sIL-6R) levels by enzyme-linked immunosorbent assay in kidney allograft recipients with acute, chronic or stable graft evolution. The percentage of CD4 and CD8 T cells in transplanted patients was lower than in the control group (P < 0.001) with the exception of CD8 gammadelta T cells from patients with stable evolution (P > 0.05). The serum levels of IL-6 and sIL-6R in acute and chronic rejection were higher than in the controls (P < 0.05). No differences in IL-6 levels were observed between the stable evolution and the control groups (P > 0.05). The levels of sIL-6R were higher in stable evolution patients than in the controls (P < 0.05) and no differences were observed between the chronic and stable evolution patients (P > 0.05). IL-6 decreased in patients with a favourable evolution, increased in those with an increased renal dysfunction and was maintained when the renal dysfunction was not modified. These results suggest that gammadelta T cells could participate in renal allograft maintenance and that IL-6 but not sIL-6R serum levels may provide a prognostic marker for measuring the evolution of kidney allograft.     

Elevated plasma amylase levels in advanced chronic heart failure secondary to ischemic or idiopathic dilated cardiomyopathy: correlation with circulating interleukin-6 activity.

It has been reported that proinflammatory cytokine activation is associated with both mesenteric venous congestion and peripheral tissue underperfusion in advanced chronic heart failure. The aim of our study was to investigate if plasma amylase (as an easily approached marker of a low-grade peripheral organ injury caused by elevated systemic venous pressure and reduced cardiac output) is elevated in severe heart failure and if this elevation is correlated with cytokine and neurohormonal activation in the plasma of heart failure patients. Plasma levels of amylase, tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor (GM-CSF), norepinephrine, and renin activity were measured in 43 severe heart failure patients (ischemic, 28; dilated, 15; left ventricular ejection fraction [LVEF] 27 +/- 3%; New York Heart Association [NYHA] classes III-IV), in 37 mild heart failure patients (ischemic, 26; dilated, 11; LVEF, 33 +/- 5%; NYHA classes I-II), and in 20 age-matched and gender-matched healthy controls. NYHA III-IV heart failure patients exhibited significantly higher plasma levels of amylase (342 +/- 19 vs. 174 +/- 13 U/L, p < 0.01), TNF-alpha (6.2 +/- 0.5 vs. 4.2 +/- 0.3 pg/ml, p < 0.01), IL-6 (5.9 +/- 0.3 vs. 4.4 +/- 0.3 pg/ml, p < 0.05), GM-CSF (21.2 +/- 2.7 vs. 4.1 +/- 0.9 pg/ml, p < 0.001), and neurohormones (both p < 0.001) compared with NYHA I-II heart failure patients and healthy controls (amylase, 165 +/- 11 U/L, p < 0.01; TNF-alpha, 2.7 +/- 0.3 pg/ml, p < 0.001; IL-6, 3.2 +/- 0.2 pg/ml, p < 0.01; GM-CSF, 3.1 +/- 0.7 pg/ml, p < 0.001). Only in NYHA III-IV heart failure patients, plasma amylase levels were significantly correlated with plasma IL-6 activity (r = 0.86, p < 0.001), plasma norepinephrine levels (r = 0.82, p < 0.001) and right atrial pressure (r = 0.52, p < 0.05). Additionally, circulating IL-6 was also significantly correlated with plasma norepinephrine (r = 0.86, p < 0.001) and right atrial pressure (r = 0.57, p < 0.01). In conclusion, plasma amylase levels were elevated in severe heart failure patients and correlated well with circulating IL-6 activation, possibly as a result of both mesenteric venous congestion and impaired peripheral tissue perfusion observed in advanced chronic heart failure. However, the lack of association between plasma IL-6 and amylase levels in mild heart failure patients indicates an independent correlation of each variable with the functional status of the disease.     

Effect of low-dose cyclosporin a microemulsion on disease severity, interleukin-6, interleukin-8 and tumor necrosis factor alpha production in severe pediatric atopic dermatitis

BACKGROUND: The release of cytokines [interleukin-6 (IL-6), IL-8 and tumor necrosis factor-alpha (TNF-alpha)] by skin cells is involved in the pathogenesis of atopic dermatitis (AD). Objective: To evaluate the effect of low-dose cyclosporin A (CyA) on clinical symptoms and cytokine secretion in severe pediatric AD. METHODS: Ten children with severe AD (SCORAD index >50) were treated for 8 weeks with CyA. The initial dose of 2.5 mg/kg/day was titrated to a maximum of 5 mg/kg/day until a SCORAD reduction of >or =35% was achieved ("treatment response"). After stopping CyA all patients entered a 4-week follow-up period. Cytokine secretion (IL-6, IL-8 and TNF-alpha) from patients' PBMC was assessed by ELISA before and after CyA treatment and was compared with 18 healthy nonatopic controls. Only the data of patients, who responded to CyA and did not experience a relapse during the follow-up period, were evaluated for this paper. RESULTS: Seven patients responded to CyA without relapse during the follow-up period. The median SCORAD index in these patients improved from 71 at baseline to 22 after CyA treatment (p < 0.001). AD patients' PBMC produced more IL-6, IL-8 and TNF-alpha than PBMC of controls. Suppression of IL-6 (p < 0.05) and IL-8 (p < 0.05) production was observed after CyA treatment. TNF-alpha levels were unchanged by CyA in all patients. CONCLUSIONS: The reduction in severity of pediatric AD with CyA is associated with decreased production of IL-6 and IL-8, but not TNF-alpha by PBMC.     

Association between plasma interleukin-18 levels and liver injury in chronic hepatitis C virus infection and non-alcoholic fatty liver disease

There is significant upregulation of interleukin-18 (IL-18) expression in viral infectious diseases and in some chronic hepatic diseases, especially (i) hepatitis C virus (HCV) infection, (ii) HCV infection with persistently normal ALT levels (PNAL), and (iii) non-alcoholic fatty liver disease (NAFLD). The aim of this study was a better understanding of the implications of plasma IL-18 levels in the above-mentioned liver diseases. Thirty-four patients with HCV infection, 13 with NAFLD, and 10 controls were enrolled. The HCV-RNA and HCV-genotypes and the serum or plasma levels of IL-18, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (gamma-GT), alkaline phosphatase, total cholesterol, triglycerides, alpha(1)-fetoprotein, and ferritin were evaluated. Patients with HCV showed higher levels of IL-18 than the NAFLD patients (p <0.01) and the controls (p <0.005). Patients with NAFLD showed higher values of body mass index and liver disease parameters, compared to HCV-infected subjects or controls. These data confirm previous reports of enhanced expression of IL-18 in patients with HCV and NAFLD, compared to healthy subjects, and suggest that IL-18 is important as a marker of liver diseases.     

Prolonged elevation of interleukin-8 and interleukin-6 concentrations in plasma and of leukocyte interleukin-8 mRNA levels during septicemic and localized Pseudomonas pseudomallei infection.

Patients suffering from serious bacterial infection present to the hospital after early inflammatory events, such as release of tumor necrosis factor (TNF), have been initiated. The role of other cytokines, such as interleukin-8 (IL-8), a neutrophil chemoattractant and activator, in the pathophysiology of human sepsis is not well characterized, and there are only limited data on IL-6. We studied serial concentrations of TNF, IL-6 (involved in the acute-phase response), and IL-8 in plasma and leukocyte levels of mRNA for these cytokines in patients with localized and septicemic Pseudomonas pseudomallei infection on admission to the hospital and during a prolonged recovery phase (up to 30 days). Of 18 patients, 8 had detectable plasma IL-8 and all had raised plasma IL-6 concentrations. In patients who died median initial concentration of IL-8 (167 pg/ml; range, 97 to 362 pg/ml) and IL-6 (4,800 pg/ml; range, 60 to 9,245 pg/ml) in plasma were higher than those in survivors (P less than 0.008 and P = 0.007, respectively). Septic patients who survived and patients with localized disease had similar cytokine levels. Plasma IL-8 and IL-6 concentrations were elevated throughout the inpatient period of recovery. Circulating leukocytes contained mRNA for IL-8 but not for IL-6 and TNF, and they may secrete IL-8. An elevated plasma IL-6 concentration (greater than 1,000 pg/ml) had 75% mortality) was the best predictor of mortality in P. pseudomallei sepsis. Fifty percent of patients with detectable plasma IL-8 concentrations died. In contrast, plasma TNF bioactivity did not relate to outcome; 75% of patients who did never had detectable plasma TNF activity.     

Effect of ascorbic acid deficiency on serum ferritin concentration in patients with beta-thalassaemia major and iron overload.

The incidence of ascorbic acid (AA) deficiency and its effect on serum ferritin concentration relative to body iron stores was studied in 61 unchelated patients with beta-thalassaemia major. Thirty-nine (64%) of patients had subnormal leucocyte ascorbate concentrations without clinical evidence of scurvy. The lowest leucocyte ascorbate concentrations tended to occur in the most transfused patients. No correlation was found between the units transfused and serum ferritin concentration in the AA-deficient patients but a close correlation (r = +0.82; p less than 0.005) existed for the AA-replete group. Similarly a close correlation (r = +0.77; p less than 0.005) was obtained between liver iron concentration and serum ferritin in AA-replete patients but only a weak correlation (r = +0.385; p less than 0.025) existed for the AA-deficient group. When AA-deficient patients were treated with ascorbic acid, serum iron and percentage saturation of iron binding capacity rose significantly; serum ferritin rose in 13 of 21 patients despite the simultaneous commencement of desferrioxamine therapy. In contrast all three measurements tended to fall in AA-replete patients with ascorbic acid and desferrioxamine therapy. Thus, AA deficiency is commonly present in beta-thalassaemia patients with iron overload and may give rise to inappropriate serum ferritin concentrations in relation to body iron stores.     

Serum Pro-hepcidin Levels in Rheumatoid Arthritis and Systemic Lupus Erythematosus

Hepcidin is a principal iron regulatory hormone and its expression is stimulated by cytokines. The aim of this study was to determine serum levels of the prohormone form of hepcidin, pro-hepcidin, in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The study included 72 RA and 28 SLE patients and 33 healthy controls (HC). Serum iron status, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and pro-hepcidin levels were determined. Pro-hepcidin levels in the RA group was higher than SLE and HC groups (p < 0.05, p < 0.001, respectively). Pro-hepcidin levels did not correlate with disease activity scores, cytokine levels and serum iron status in the RA and SLE groups, while it correlated with TNF-alpha, IL-6 and ferritin levels in the HC group (r = 0.459, p < 0.01, r = 0.374, p < 0.05, r = -0.603, p < 0.01, respectively). Pro-hepcidin levels show extremely wide variations within the groups as do iron status and cytokines. Despite these wide variations correlation analysis do not reveal anything.     

Plasma interleukin-8, interleukin-10, and E-selectin levels in neutropenic and non-neutropenic bacteremic patients

Plasma interleukin-8 (IL-8), interleukin-10 (IL-10), and E-selectin concentrations were studied in 39 neutropenic and 30 non-neutropenic bacteremic patients; 54 nonbacteremic patients were analyzed as controls. Interleukin-8 concentrations were significantly higher in neutropenic than in non-neutropenic bacteremic patients (median 475 vs. 0 pg/ml, p<0.0001). Median IL-8 and IL-10 levels were higher in bacteremic than in non-bacteremic patients (330 vs. 0 pg/ml, p<0.0001 and 20 vs. 0 pg/ml, p=0.04, respectively). In contrast, concentrations of IL-10 were similar in neutropenic and non-neutropenic patients. Median levels of E-selectin were not increased in any of the patient groups. Neutropenic bacteremic patients showed significantly lower concentrations of E-selectin than did non-neutropenic bacteremic patients (p<0.0001). In conclusion, neutropenic bacteremic patients had significantly higher concentrations of IL-8 than non-neutropenic bacteremic patients. Levels of IL-10 were higher in bacteremic than in nonbacteremic patients, but neutropenic and non-neutropenic patients had similar levels of IL-10. Increased levels of E-selectin were not found in any of the patient groups, although neutropenic patients with bacteremia had lower concentrations than did non-neutropenic patients.     

Anti-CagA immunoglobulin G responses correlate with interleukin-8 induction in human gastric mucosal biopsy culture

Helicobacter pylori persists in the human stomach despite eliciting both cellular and humoral immune responses and inducing proinflammatory cytokines. To determine whether local humoral and cytokine responses are related to each other and to histologic responses, we studied 66 Japanese patients who underwent gastroscopy. Using specific enzyme-linked immunosorbent assays, we examined gastric antral mucosal-organ biopsy culture supernatants to assess interleukin-6 (IL-6) and interleukin-8 (IL-8) levels and antibody responses to H. pylori whole-cell antigens CagA, HspA, and HspB. Of the patients studied, 11 were H. pylori negative and 55 were H. pylori positive; by PCR, all strains were cagA(+). As expected, compared to H. pylori-negative patients, H. pylori-positive patients had significantly higher humoral responses to all H. pylori antigens and had higher IL-8 (47.8+/-3.5 versus 10.1+/-4.3 ng/mg of biopsy protein; P<0.001) and IL-6 levels (2.8+/-0.3 versus 0.26+/-0.2 ng/mg of protein; P<0.001). Among the H. pylori-positive patients, supernatant anti-CagA immunoglobulin G (IgG) levels were significantly associated with H. pylori density (P<0.005) and neutrophil infiltration (P<0.005) scores. Anti-CagA immunoglobulin A levels were correlated with intestinal metaplasia (P<0.05). Mononuclear cell infiltration scores were significantly associated with supernatant IL-6 levels (P<0.005) and with IgG responses to whole-cell antigens (P<0.05). Supernatant IL-8 levels were significantly associated with anti-CagA IgG (r = 0.75, P<0.001). Anti-CagA responses correlated with neutrophil infiltration, intestinal metaplasia, H. pylori density, and IL-8 levels, suggesting that the absolute levels of these antibodies may be markers for gastric inflammation and premalignant changes in individual hosts.     

Evaluation of tumor necrosis factor-α, interleukin-6 and C-reactive protein plasma levels as predictors of bacteremia in patients presenting signs of sepsis without shock

Objective: To evaluate the sensitivity of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) plasma measurement to detect bacteremia in patients presenting sepsis signs, and to evaluate the potential benefit of such measurement in terms of early antimicrobial therapy initiation.
Method: Plasma was obtained from 166 hospitalized patients for whom blood cultures were drawn for sepsis. Clinical data and antimicrobial therapies were noted. IL-6, TNF and C-reactive protein (CRP) were measured. The sensitivities of these markers were retrospectively compared with the accuracy of the attending physician in initiating empirical antimicrobial therapy. The setting was an 850-bed university hospital.
Results: Thirty-four bacteremias and 69 non-bacteremic infections were noted. In 63 others, no infection was documented. Median (range) IL-6 plasma levels in the three groups of patients were 462 (15–50 850), 189 (<15–38 300) and 91 (<10–13 750) pg/mL, respectively ( p <0.01). The corresponding TNF-α plasma levels were 37.5 (<15–2400), 15 (<15–240) and 15 (<15–200) pg/mL, respectively ( p <0.01). CRP plasma levels were 10.7 (<0.6–30.2), 10.3 (<0.6–34.4) and 7.3 (<0.6–20.9) mg/dL, respectively ( p =0.12). With respect to these three parameters, IL-6 and TNF-α appear better than CRP for predicting bacteremia. Clinical features resulted in starting empirical antimicrobial therapy in only 62% of the bacteremic patients. On the other hand, 68% of these bacteremic patients had high IL-6 plasma levels (>200 pg/mL). A combination of clinical features and high IL-6 levels would have permitted early treatment for 82% of the bacteremic patients.
Conclusions: IL-6 and TNF-α thus appear to be useful and earlier markers of bacteremia in septic patients. By contrast, CRP is neither sensitive nor specific in this setting.     

Seminal plasma components stimulate interleukin-8 and interleukin-10 release.

Human seminal plasma has potent anti-inflammatory properties which are thought to confer a survival advantage to the spermatozoa within the hostile female genital tract. In contrast, a profound pro-inflammatory leukocytosis has been observed post-coitus in animals and humans. Whether components of seminal plasma are involved in initiating this leukocytic reaction is not known. This study investigated the effect of human seminal plasma, a seminal plasma fraction and its principal constituent prostaglandins, prostaglandin E2 (PGE2) and 19-hydroxy PGE, on the release of the pro-inflammatory neutrophil chemotactic factor interleukin-8 (IL-8) and the anti-inflammatory cytokines interleukin-10 (IL-10) and secretory leukocyte protease inhibitor (SLPI). The tissues studied were non-pregnant cervical explants, peripheral blood and the monocyte cell line U937. Seminal plasma fraction (SPF) significantly (P < 0.05) stimulated release of IL-8 and inhibited release of SLPI from non-pregnant cervical explants. SPF, PGE2 and 19-hydroxy PGE significantly (P< 0.005) stimulated IL-8 release from peripheral blood and U937 cells. 19-hydroxy PGE was significantly (P< 0.005) more effective than PGE2 in stimulating IL-8 release. Seminal plasma, SPF and PGE2 significantly (P < 0.05) stimulated IL-10 release from U937 cells. 19-hydroxy PGE stimulated IL-10 release from U937 cells but this failed to reach significance. Release of IL-10 by cervical explants and SLPI by peripheral blood and U937 cells were below the detection limit of the assays employed. We suggest that the anti- and pro-inflammatory immune responses which seminal plasma induces might act in combination initially to promote sperm survival and then to facilitate their removal from the female genital tract.     

用HB-H-6树脂血浆灌流清除细胞因子治疗银屑病的临床研究

目的观察血液灌流治疗严重银屑病患者细胞因子的变化及与临床疗效的关系。方法选择5例银屑病患者,其中男性4例,女性1例,平均年龄32.1岁。均伴有重型肝炎或药物性肝损伤。在常规药物治疗基础上进行血浆灌流治疗,灌流前后分别取患者血浆,测定肿瘤坏死因子α（TNF-α）、白细胞介素1（IL-1）、白细胞介素6（IL-6）和白细胞介素8（IL-8）,检测其他相关生物化学、临床指标并观察记录临床表现情况。结果血液灌流前后比较,TNF-α、IL-1、IL-6和IL-8均显著下降（P〈0.05）,血浆胆红素显著下降（P〈0.05）,其他生物化学及临床指标变化不明显,患者临床治疗效果明显。结论血液灌流能吸附严重银屑病患者血浆中的TNF-α、IL-1、IL-6和IL-8,能明显改善临床症状,可以成为严重银屑病的新的治疗手段。     

Serum levels of interleukin-6 and interleukin-10 in relation to depression scores in patients with cardiovascular risk factors

It is currently unknown whether elevated cytokine levels in depression are confined to any specific subgroup of depressive patients. In this study, medical out-patients presenting with cardiovascular risk factors (N = 356) were assessed for both cognitive-affective and physical symptoms of depression using the Hospital Anxiety and Depression Scale (HADS) and the Maastricht questionnaire (MQ), respectively. In study participants assigned to the highest (≥21) and lowest (≤5) quartile for the MQ score, serum levels of cytokines were measured. We found highly significant associations between cognitive-affective symptoms of depression and elevated serum levels of interleukin-6 (IL-6; ρ = .231; p = .002) and interleukin-10 (IL-10; ρ = .370; p < .001), respectively. In multiple regression models elevated IL-10 serum concentration was independently related to cognitive-affective symptoms of depression (ρ = .165; p = .002). When all cytokines were included in one model, elevated IL-10 serum concentrations remained a significant predictor for depressive mood (ρ = .157; p = .009). In patients with cardiovascular risk factors and extreme scores for vital exhaustion, elevated serum IL-6 and even more IL-10 concentrations are linked to the presence of depressive mood. Future studies will have to test whether the so far unreported association of IL-10 with depressive mood represents a causal pathway involved in the pathogenesis or in the prognostic effect of depressive mood in cardiac patients.     

兔深静脉血栓形成与血浆单核细胞趋化蛋白4及白细胞介素8的水平

背景：关节置换后深静脉血栓形成的预后在个体间存在很大的差异。有研究表明,巨噬细胞和内皮细胞活性的增高对于血栓溶解管腔再通有促进作用。 目的：分析兔深静脉血栓形成后不同时段血浆单核细胞趋化蛋白4及白细胞介素8质量浓度对于反映血栓病情有无特异性。 方法：新西兰大白兔78只,随机分为血栓组、假手术组及正常对照组,血栓组造模后14 d根据血栓再通情况分为再通组及未通组。分别于血栓后8 h,3 d,7 d,14 d抽取耳缘静脉血行单核细胞趋化蛋白4、白细胞介素8质量浓度测定和血常规检测。 结果与结论：血栓后第7天血浆单核细胞趋化蛋白4质量浓度再通组较未通组有显著升高(P < 0.01),白细胞介素8质量浓度再通组较未通组降低(P < 0.05)。其变化与单核细胞、中性粒细胞之间无相关性(P > 0.05)。结果表明血栓形成后血浆高质量浓度的单核细胞趋化蛋白4的病例血栓再通情况较好。单核细胞趋化蛋白4的质量浓度通过反映巨噬细胞和内皮细胞的活性,在一定程度上反映了深静脉血栓形成的预后。     

Circulating interleukin 10 and interleukin-6 serum levels in rheumatoid arthritis patients treated with methotrexate or gold salts: Preliminary report

In order to evaluate the relationship between serum concentrations of interleukin-10 (IL-10), IL-6, and acute phase proteins in rheumatoid arthritis (RA) patients treated with methotrexate (MTX) or intramuscular gold (IMG) we determined IL-10, IL-6, C-reactive protein (CRP), alpha-1-acid glycoprotein (AGP) and alpha-1-antichymotrypsin (ACT) in the sera of 35 RA patients. IL-10 and IL-6 levels were evaluated using an enzyme-linked immunoassay (ELISA). AGP and ACT level were measured using rocket immunoelectrophoresis. IL-10 serum level was not increased in RA patients as compared to controls (58.7 ± 18.1 pg/ml vs. 57.2 ± 11.9 pg/ml). IL-6 level was significantly elevated (91.6 ± 46.9 pg/ml vs. 45 ± 19 pg/ml, p < 0.05). CRP was significantly increased as compared to healthy controls (35 ± 19 mg/l vs. 3 ± 2 mg/l, p < 0.05). Patients treated with MTX or IMG presented an increased level of IL-10 and decreased amounts of IL-6, as compared to those treated with NSAID only. However, only changes between patients treated with IMG and NSAID were found to be statistically significant. A good negative correlation between IL-10 and IL-6 serum level was found (r = –0.75, p < 0.05). A positive significant correlation between IL-6 serum level and CRP (r = 0.62, p < 0.05), AGP (r = 0.78, p < 0.05) and ACT (r = 0.45, p < 0.05) was established. On the other hand, a negative correlation between IL-10 and serum level of CRP (r = –0.76, p < 0.05), AGP (r = –0.64, p < 0.05) and ACT (r = –0.38, p < 0.05) was also observed. Moreover, these relationships were maintained when patients treated with MTX, IMG, or NSAID were analyzed independently. According to the data thus far obtained, it seems that IL-10 decreases IL-6 production, and thereby indirectly affects the acute phase response, decreasing CRP, AGP, and ACT concentration in RA patients.Abbreviations ACT -1-antichymotrypsin - AGP ₁-acid glycoprotein - APP acute phase protein - CRP C-reactive protein - CSF colony stimulating factor - IFN interferon - IL interleukin - IMG intramuscular gold - MTX methotrexate - NSAID non-steroidal anti-inflammatory drug - RA rheumatoid arthritis     

Studies on circulating interleukin-6 and thyroid functions in acute myocardial infarction

The euthyroid sick syndrome is reported to exist in acute myocardial infarction(AMI). Previous reports showed serum levels of triiodothyronine(T3) are low and thyroid stimulating hormone(TSH) is normal or subnormal levels in patients with AMI. However, the mechanism of altered thyroid hormone metabolism is unknown. Interleukin-6(IL-6) is reported to be a key role in the pathogenesis of AMI and euthyroid sick syndrome. We measured circulating TSH, free T3(FT3), free thyroxine (FT4), IL-6, soluble IL-6 receptor, soluble transducing 130-kD glycoprotein, atrial natriuretic peptide(ANP) and brain natriuretic peptide in 25 patients and 32 healthy subjects. Circulating FT3 levels in patients with AMI became lower than in control group(p < 0.05). IL-6 levels were significantly(p < 0.05) higher than those of healthy subjects. The peak levels of IL-6 was 30.5 +/- 46.9 pg/ml at 25-27 hours(the first peak) and 64.4 +/- 24.6 pg/ml at 70-72 hours(the second peak). FT3 was negatively related to IL-6(p < 0.05) and hANP(p < 0.05) in patients with AMI. These results indicate that the lower levels of FT3 show the greater severity of AMI. We conclude that euthyroid sick syndrome occurs in patients with AMI and euthyroid sick syndrome may regulated by IL-6 through suppressed of thyroid function.     

急性颅脑损伤后脑脊液中IL-6和IL-8的变化及临床意义

目的研究急性颅脑损伤后脑脊液中白细胞介素-6（IL-6）和白细胞介素-8（IL-8）含量的变化规律,探讨其含量变化与损伤程度、预后的关系。方法对54例急性颅脑损伤患者以GCS评分分组,分别检测不同时段脑脊液中IL-6、IL-8的含量。结果急性颅脑损伤后第1天脑脊液中IL-6、IL-8含量显著升高,第3天降至最低（P〈0.01）。轻、中型颅脑损伤组脑脊液中IL-6含量与重型颅脑损伤组相比无显著差异（P〉0.05）;而脑脊液中IL-8含量在两组间有显著性差异（P〈0.01）。脑脊液中IL-6、IL-8含量在存活组和死亡组间有显著性差异（P〈0.01）。结论IL-6、IL-8参与了颅脑损伤的病理生理过程,对指导治疗、判断伤情和预后有重要意义。     

Neuropeptides and interleukin-6 in human joint inflammation. Relationship between intraarticular substance P and interleukin-6 concentrations

Plasma and synovial fluid concentrations of interleukin-6 (IL-6), using an enzyme-linked immunosorbent assay, as well as immunoreactive levels of calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal peptide (VIP) were measured in 18 patients with rheumatoid arthritis and 20 with osteoarthritis of the knee. The concentrations of IL-6 were elevated in both plasma and synovial fluids from patients with rheumatoid arthritis whereas higher levels of substance P-, CGRP- and VIP-like immunoreactivities were found in the synovial fluid, but not in plasma, from patients with rheumatoid arthritis when compared with those in osteoarthritis. Furthermore, IL-6 and substance P levels in synovial fluid were significantly correlated both in rheumatoid arthritis and osteoarthritis patients. Our data seem to support the idea of an important role shared by neuropeptides and IL-6 in the pathogenesis of human inflammatory joint disease.