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Journal Article 2006; 27(1-2): 183-188 PubMed PMID: 16648806 Citation  Keywords:  Absorptiometry, Photon, Acromegaly:blood, Adult, Aged, Body Mass Index, Bone Density:physiology, Cytokines:blood, Enzyme-Linked Immunosorbent Assay, Female, Human Growth Hormone:blood, Humans, Male, Middle Aged, Sex Characteristics, Testosterone:blood,.   

OBJECTIVES: Elevated cytokines levels were observed as a marker of increased bone resorption in certain diseases. The aim was to assess serum levels of selected cytokines in acromegaly, regarding to different disease's stages, gonadal function, gender and character of BMD change.

METHODS: The study was carried out in 62 patients with acromegaly (40 women, 22 men) aged 26-75 years in various stages of the disease. The controls were 30 healthy, age- and sex-matched subjects. Serum cytokines concentration was assessed using ELISA method.

RESULTS: We have shown higher (p=0.044) concentrations of TGF-beta in male patients with active acromegaly than in cured males. When the influence of all cytokines studied on BMD using multiple regression analysis was carried out, the borderline (p=0.099) statistical significance was achieved (regression coefficient B=0.68271) according to TGF-beta and trochanter major BMD. IL-6 and TNF-alpha were higher (p=0.062, and p=0.098, respectively) in these acromegalic patients, in which gain of trochanter major BMD occurred. IL-1beta levels were lower in patients with ultradistal radius and 1/3 distal radius BMD gain (p=0.007, and p=0.009, respectively). Lower TGF-beta levels (p=0.077) were shown in patients with 1/3 distal radius gain. IL-6 levels were higher in patients with total body BMD gain (p=0.059).

CONCLUSIONS: The relations between TGF-beta and acromegaly activity in men, and trochanter major BMD in both sexes were documented. Concentrations of all cytokines studied correlated with the BMD changes in different bone sites. Noteworthy is homogeneity of the secretory character of cytokines studied according to BMD changes within particular skeleton sites....

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Comparative Study 2005; 26(6): 739-744 PubMed PMID: 16380673 Citation  Keywords:  Analysis of Variance, Animals, Arthritis, Experimental:chemically induced, Arthritis, Rheumatoid:enzymology, Chemokine CCL5:genetics, Collagen, Cytokines:genetics, Disease Models, Animal, Down-Regulation, Female, Interleukin-1:genetics, Interleukin-6:gene.   

OBJECTIVE: To observe the effects and mechanisms of beta-endorphin (beta-END) preventing collagen induced arthritis (CIA) by neuroimmuno-regulating pathway.

METHODS: Female wistar (Ws) rats were used in this study. CIA was induced by Native bovine type II collagen emulsified with complete Freund's adjuvant (CFA). Beta-END was administered i.p. to CIA rats every other day from the 14th day (secondary immunization) to the 35th day after primary immunization. Clinical assessments were performed by two independent, blinded examiners every other day. Pathological and radiological observations were taken on the 35th day after the primary immunization. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), regulated upon activation, normal T-cell expressed and secreted (RANTES), inducible NO syntheses (iNOS), matrix metalloproteinase-2 (MMP-2) and MMP-9 mRNA expression of synovium tissues of CIA rats was estimated by quantitative RT-PCR. The frequency of spleen Th1 and Th2 cells were assessed by fluorescence activated cell sorter (FACS) assay.

RESULTS: Clinical manifestation of rats with CIA were significantly abrogated or ameliorated by treatment with beta-END. Beta-END treatment in vivo could down-regulate mRNA expression of several pro-inflammatory cytokines, chemokines and MMPs in CIA synovial, and polarize Th1/Th2 balance to Th2.

CONCLUSION: Beta-END alleviates CIA through both depressing Th1 responses and down-regulating proinflammatory and other rheumatic factors, suggesting beta-END is a promising anti-inflammatory and anti-rheumatic agent in treating CIA....

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Clinical Trial 2005; 26(5): 473-479 PubMed PMID: 16264416 Citation  Keywords:  Acute-Phase Reaction:physiopathology, Adipose Tissue:physiology, Adolescent, Anthropometry, Biomarkers, Blood Glucose:metabolism, Body Composition:physiology, Child, Cytokines:blood, Endothelium, Vascular:physiology, Female, Hemoglobin A, Glycosylated:met.   

OBJECTIVES: There is increasing evidence that an ongoing cytokine-induced acute-phase response is closely involved in the pathogenesis of type 2 diabetes and associated complications such as dyslipidemia and atherosclerosis. The aim of this study was to investigate the relationship of inflammation and endothelial activation with insulin resistance in childhood obesity.

METHODS: Two hundred and eleven (122 boys) obese children and adolescents were examined. Fasting levels of ultra-sensitive C-reactive protein (CRP), fibrinogen (FB), interleukin-6 (IL-6), interleukin-1beta (IL-1beta), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), von Willebrand factor (vWF), glucose, insulin, and HbA1c were determined. Insulin resistance was assessed by the homeostasis method.

RESULTS: HOMA IR correlated significantly with all measures of adiposity as well as with majority of inflammation and endothelial dysfunction markers. After adjustment for age, gender, BMI and fat mass, the correlation with insulin resistance remained significant for CRP, ICAM-1 and von Willebrand factor. There was a trend for association between HOMA IR and IL-6 as well as HOMA IR and fibrinogen.

CONCLUSION: Acute-phase reaction and endothelial activation correlate with insulin resistance in obese youth. It is possible that the cluster of these pro-atherogenic factors may contribute to the accelerated atherosclerosis in obese children....

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Journal Article 2005; 26(3): 231-236 PubMed PMID: 15990727 Citation  Keywords:  Animals, Brain Chemistry:immunology, Cell Extracts:chemistry, Cytokines:analysis, Detergents, Enzyme-Linked Immunosorbent Assay:methods, Interferon-gamma:analysis, Interleukin-10:analysis, Kidney:chemistry, Lipopolysaccharides:pharmacology, Liver:chemistr.   

OBJECTIVES: Determination of protein cytokines in local tissues would help to evaluate their local role in health, sickness behavior and immune-mediated diseases. Therefore, developing a simple quantitative method of protein cytokines in tissues/organs is highly important.

METHODS: Mouse tissues were collected following intraperitoneal administration of endotoxin-free PBS or lipopolysaccharide. A mild detergent, 0.1% Igepal, was added in a buffer to enhance cytokines extraction. The tissues were then disrupted, homogenized, centrifuged and the supernatants were collected and assayed using solid-phase immunoassays.

RESULTS: The presence of 0.1% Igepal extracted significantly more TNF-alpha from liver (322%: p<0.01), brain (358%: p<0.05), lungs (1600%: p<0.01), and more IL-10 from liver (220%: p<0.001), brain (4650%: p<0.001) than PBS alone. On the other hand, using 0.1% Igepal did not increase IFN-gamma extraction from liver, spleen, brain, lungs, skin and kidneys more than PBS alone. Furthermore, i.p. administration of LPS induced a differential milieu of cytokines. LPS increased significantly the production of TNF-alpha, IFN-gamma, and IL-10 from liver (521%, 123%, 72%: p<0.01, 0.04, 0.04), brain (470%, 122%, 280%: p< 0.01, 0.03, 0.01), peritoneal lavage (p<0.001) and blood (p<0.001). However, the pattern of increase was different for the above cytokines in spleen, skin, lungs and kidneys.

CONCLUSIONS: The extraction of protein cytokines from tissues was superior with addition of mild detergent. Furthermore, our results showed a differential cytokines response to LPS with respect to tissue and cytokine type. This method should provide an important tool for studying local protein cytokines in behavioral pattern, sickness behavior, and immune-mediated diseases as well as to determine local therapeutic efficacy of immunomodulatory drugs....

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Clinical Trial 2004; 25(5): 356-360 PubMed PMID: 15580170 Citation  Keywords:  Adenoma:metabolism, Cytokines:blood, Hepatocyte Growth Factor:blood, Humans, Hyperplasia, Insulin-Like Growth Factor I:analysis, Parathyroid Glands:metabolism, Parathyroid Neoplasms:metabolism, Reference Values, Transforming Growth Factor beta:blood,.   

INTRODUCTION: HGF (Hepatocyte Growth Factor), TGFbeta1 (Transforming Growth Factor beta1) and IGF-I (Insulin Like Growth Factor I) are cytokines that are involved in the parathyroid tumors formation and growth. We tried to determine, if there are changes and relationships in the production of these cytokines by tumor cells of parathyroid tumors.

MATERIAL AND METHODS: We determined concentrations of HGF, TGFbeta1 and IGF-I in serum from peripheral blood of 16 patients with parathyroid adenoma and of 8 patients with parathyroid secondary hyperplasia before and after parathyroidectomy. Results were compared with serum levels in healthy people.

RESULTS: Both preoperative and postoperative HGF serum levels in patients with parathyroid adenoma and secondary hyperplasia are significantly higher than in healthy people. Preoperative and postoperative serum levels of TGFbeta1 in parathyroid adenoma and postoperative TGFb1 serum levels in parathyroid secondary hyperplasia are higher, compared with those in the healthy population and in parathyroid secondary hyperplasia preoperatively. There are no significant differences of IGF-I serum levels among the all investigated groups of patients.

CONCLUSIONS: Changes in the growth factors production by parathyroid tumor cells are reflected by their concentrations in peripheral blood. The elevation of HGF serum levels in patients with parathyroid adenoma and hyperplasia can be explained by very high HGF production by tumor cells. Nevertheless, there is no decrease of HGF serum levels after the parathyroidectomy. That may be the result of the extratumoral production of this cytokine. Also TGFbeta1 and IGF-I serum levels indicate high possibility of the extratumoral production of these cytokines. Higher postoperative IGF-I serum levels (but not significantly) in parathyroid secondary hyperplasia are in accordance with its bone production....

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Journal Article 2003; 24(5): 283-292 PubMed PMID: 14646999 Citation  Keywords:  Cytokines:physiology, Humans, Neuroimmunomodulation:physiology, Neurosecretory Systems:immunology, Stress, Psychological:immunology, Time Factors,.   

OBJECTIVES: Previously, a large number of studies reported that psychological stress and psychiatric illness reduces immune responsiveness. However, it turned out that stress reduces immune responsiveness is an oversimplified statement because the interactions between central nervous system, endocrine system and the immune system are undoubtedly complex. Therefore, this study aims in reviewing mental stress models (e.g. brief and written examination stress as subacute and acute type of stressor) that have been utilized to understand the effect of stress on the neuroendocrine and immune systems.

METHODS: The published findings from human mental stress models on catecholamines, cortisol, prolactin levels and on T helper (Th) 1 and 2-induced cytokines are presented and discussed with respect to the in vitro and in vivo effects of glucocorticoids, catecholamines, and prolactin on the induction of cytokines.

RESULTS: This review shows evidence that short-time (minutes) or preparation to a written examination, in those students who are stressed, induces the production of proinflammatory cytokines which may be related to Th1 response. However, longer mental stress (days) causes dysregulation in the immune function by shifting the cytokine response to Th2 response.

CONCLUSIONS: The outcome from neuroendocrine and immune function prior to, following and after mental stress depends on multiple variables most importantly on the amount of stress, exposure time, coping behavior and adjustment of the individual. A few minutes of stress may improve immune performance but longer times of mental stress have detrimental effects that may lead to loss of immune integrity. Furthermore, studies on stress and common heath problems are necessary to increase our knowledge and understanding of the mechanisms responsible for producing neuroendocrine-induced immune changes in health and common diseases....

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Journal Article 2003; 24(3-4): 185-191 PubMed PMID: 14523355 Citation  Keywords:  Cytokines:biosynthesis, Dose-Response Relationship, Drug, Estradiol:pharmacology, Female, Humans, Hydrocortisone:antagonists & inhibitors, In Vitro Techniques, Indicators and Reagents, Interferon-gamma:biosynthesis, Interleukin-10:biosynthesis, Interleuki.   

OBJECTIVES: The purpose of this study was to determine the effects of estradiol and progesterone on interferon-gamma (IFN-gamma), interleukin (IL)-12, IL-10 and tumor necrosis factor-alpha (TNF-alpha) productions in polyclonal activators (phytohemagglutinin+lipopolysaccharide)-stimulated whole blood cultures.

METHODS: Nineteen healthy males and females volunteered in the study. Blood samples were drawn, diluted, and cultured for 24h with different concentrations of estradiol, progesterone or hydrocortisone and then PHA+LPS was added for another 24 h. The supernatant, then, was harvested and assayed for IL-12 p70, IFN-gamma, IL-10 and TNF-alpha.

RESULTS: At preovulatory concentrations, estradiol enhanced significantly IFN-gamma, IL-12 and IL-10, but not TNF-alpha, production levels and reversed the suppressive effect of hydrocortisone in PHA+LPS stimulated whole blood. While IL-10 levels kept increasing at pregnancy estradiol concentrations, IFN-gamma, IL-12 levels and IFN-gamma/IL-10 ratio decreased significantly. No effect of progesterone on IL-12 p70, IFN-gamma, IL-10 and TNF production levels was observed.

CONCLUSIONS: The present study shows that those pregnancy estradiol concentrations (and higher) enhance the production of IL-10 and reduce IL-12, IFN-gamma levels and IFN-gamma/IL-10 ratio in stimulated whole blood cells. Because of the known IL-10 inhibitory actions on T helper (Th) 1 cells and monocytes/macrophages, these high IL-10 levels keep Th2 cytokines favored during pregnancy and may be useful in shifting Th1-mediated autoimmune diseases towards non-pathogenic Th2 pathway....

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Comment 2002; 23(1): 10-12 PubMed PMID: 11880856 Citation  Keywords:  Cytokines:physiology, Epilepsy:physiopathology, Humans,.   

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