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ABSTRACT: Regular exercise is a good non-pharmacological treatment of metabolic syndrome in that it improves obesity, diabetes, and inflammation. The 72 kDa extracellular heat shock protein (eHsp72) is released during exercise, thus stimulating the inflammatory responses. The aim of the present work was to evaluate the effect of regular exercise on the eHsp72-induced release of IL-1β, IL-6, and TNFα by macrophages from genetically obese Zucker rats (fa/fa) (ObZ), using lean Zucker (LZ) rats (Fa/fa) to provide reference values. ObZ presented a higher plasma concentration of eHsp72 than LZ, and exercise increased that concentration. In response to eHsp72, the macrophages from ObZ released less IL-1β and TNFα, but more IL-6, than macrophages from LZ. While eHsp72 stimulated the release of IL-1β, TNFα, and IL-6 in the macrophages from healthy LZ (with respect to the constitutive release), it inhibited the release of IL-1β and IL-6 in macrophages from ObZ. The habitual exercise improved the release of inflammatory cytokines by macrophages from ObZ in response to eHsp72 (it increased IL-1β and TNFα, and decreased IL-6), tending to values closer to those determined in healthy LZ. A deregulated macrophage inflammatory and stress response induced by eHsp72 underlies MS, and this is improved by habitual exercise.
International Journal of Sports Medicine 11/2012; · 2.43 Impact Factor
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ABSTRACT: It is still not really known what is the optimal level of exercise that improves, but does not impair or overstimulate the innate immune function. This is especially the case in women, who have higher basal levels of 'inflammatory markers' than men. The aim of this work was to evaluate differences in the magnitude of the stimulation of the innate/inflammatory response following a single bout of moderate or intense exercise in sedentary women, all of them in the follicular phase of their menstrual cycle. Changes in stress and sexual hormones were also evaluated.
Changes induced by exercise (45 min at 55% VO(2) max vs. 1 h at 70% VO(2) max on a cycle ergometer) in the phagocytic process (chemotaxis, phagocytosis, and microbicide capacity against Candida albicans) and in serum concentrations of IL-1beta, IL-2, IFN-gamma, IL-12, IL-6, and IL-4 (ELISA) were evaluated. Parallel determinations were also made of serum or plasma concentrations of catecholamines (HPLC) and cortisol, oestradiol, and progesterone (electrochemiluminescence immunoassay).
Both exercise intensities increased chemotaxis, phagocytosis, and microbicide capacity of the neutrophils. However, the increase in chemotaxis was greater after moderate exercise. All the cytokines assayed were affected by exercise intensity. IFN-gamma increased significantly only immediately after the intense exercise; IL-1beta increased following both exercise intensities, although at 24 h it only remained elevated after the intense exercise; IL-12 only increased 24 h after the intense exercise, and IL-2 only showed a significant decrease following the moderate exercise. IL-6 increased immediately after both exercise intensities, but more so after moderate exercise. While IL-4 (an anti-inflammatory cytokine) increased following the moderate exercise, it decreased after the intense exercise. Both moderate and intense exercise increased norepinephrine and decreased cortisol, both of which returned to basal levels after 24 h. Only the intense exercise affected the epinephrine, oestradiol, and progesterone concentrations, with increases in epinephrine and oestradiol immediately after exercise, and a decrease in progesterone after 24 h.
Both moderate and intense exercise stimulate the phagocytic process of neutrophils in sedentary women, but the profile of pro-/anti-inflammatory cytokine release seems to be better following the moderate exercise. The possible participation of stress (catecholamines and cortisol) and sex (oestradiol and progesterone) hormones in these intensity-dependent immune changes is discussed.
NeuroImmunoModulation 05/2009; 16(4):237-44. · 2.38 Impact Factor
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ABSTRACT: The purpose of the present work was to determine differences between young men (M), and women in the follicular phase (W) and women taking oral contraceptives containing ethinylestradiol (CW) in the phagocytic process of neutrophils (chemotaxis, phagocytosis and microbicide capacity), in the serum concentrations of cytokines both pro-inflammatory (IFNgamma, TNFalpha, IL-12, IL-6, IL-8) and anti-inflammatory ones (IL-10 and IL-13), and in neuroendocrine factors with immunomodulatory capacity (estradiol, prolactin, cortisol, catecolamines and 72 kDa heat shock proteins, Hsp72). Men showed a lower phagocytosis and microbicide capacity than women, and less serum concentrations of the pro-inflammatory cytokines IL-6 and IL-8. CW neutrophils also showed a lower phagocytic capacity than W neutrophils, together with less serum IL-8 concentration. CW showed the highest serum concentration of IL-13. However, no statistical changes were observed in the pro-inflammatory cytokines: INF-gamma, TNF-alpha, IL-12 and in the anti-inflammatory cytokine IL-10. The greater anti-inflammatory status in CW than in W was parallel with lower concentrations of oestrogens. Cortisol, prolactin, and the extracellular Hsp72 seem to be involved in the gender- and contraceptives-induced differences in the inflammatory response. While cortisol (in general an immunosuppressive hormone) showed the highest values in CW, prolactin and Hsp72 (an immunopermissive factors) showed the lowest values in CW and M. Less clear is the participation of catecholamines in the gender-inflammatory differences.
Molecular and Cellular Biochemistry 07/2008; 313(1-2):147-53. · 2.06 Impact Factor
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ABSTRACT: The aim of this study was to evaluate the therapeutic effect of melatonin, the main hormone of the pineal gland, on rats with advanced and untreated mammary tumours. Mammary tumours were chemically induced in Sprague-Dawley rats with the carcinogen 9,10-dimethyl-1,2-bezanthracene (DMBA). After the appearance of tumours the effect of melatonin (5 mg/ml per rat per day) was then evaluated on the survival time, tumour multiplicity, and tumour volume until the death of the animals. In addition, the variations in prolactin, noradrenaline and adrenaline concentrations, and in the percentage of NK cells were evaluated after one month of the treatment with melatonin. Daily administration of melatonin increased significantly the survival time of tumour-bearing animals (p<0.05 with respect to the control non-melatonin-receiving rats). The increased survival time did not correlate, however, with changes in either tumour multiplicity or tumour growth rate. Animals with mammary tumours exhibited an increase (p<0.05 with respect to healthy animals) in prolactin and catecholamine concentrations. The administration of melatonin stabilized the hormone levels, returning them to those in the basal-healthy animals. Rats with mammary tumours also presented lower percentages of NK cells, which were not increased by the administration of melatonin. The results strongly suggest that melatonin per se is beneficial during advanced breast cancer. It increases survival time, maybe by improving the homeostatic and neuroendocrine equilibrium which is imbalanced during advanced breast cancer.
Molecular and Cellular Biochemistry 10/2005; 278(1-2):15-20. · 2.06 Impact Factor
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ABSTRACT: Melatonin has been reported to be involved in the feedback between neuroendocrine and immune functions and to exert oncostatic actions. Likewise, this hormone seems to lengthen life span in healthy animals. As of present, most studies have analysed the therapeutic effect of melatonin on cancer growth, but few have tested the preventive effect of melatonin in reducing the risk of cancer. Thus, the aim of this study was to evaluate the preventive-therapeutic effects of melatonin on rats with DMBA-induced mammary tumours, and to examine the effect of melatonin on the first line of cell defence against cancer (macrophages and NK cells) and on some of the neuroendocrine factors that are involved in the development of tumours (prolactin and catecholamines). Melatonin treatment (5 mg/day/animal) began one month prior to DMBA (9,10-dimethyl-1,2-benzanthracene) administration to females Sprague Dawley rats. It was found that the treatment led to an increase in survival and in latency time in the tumour-bearing rats. Although the melatonin treatment did not influence either the phagocytic capacity of macrophages or the number of peripheral blood NK cells, it did stabilise the levels of prolactin by returning the concentrations of this hormone to those of the healthy animals. We conclude that melatonin can exert an oncostatic action, lengthening the survival time of mammary tumour-bearing animals, and suggest that this effect is due, at least in part, to regulating the neuroendocrine parameters of tumour-bearing animals, bringing them closer to their optimal physiological status.
Molecular and Cellular Biochemistry 02/2005; 268(1-2):25-31. · 2.06 Impact Factor
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ABSTRACT: The deterioration of the immune system with ageing, which leads to an increased morbidity and mortality from infections, appears to be related to decreases in specific lymphocyte functions. However, the alteration of non-specific immunity is a more controversial subject. Our purpose was to investigate the age-related changes of different functions of the non-specific immune response in peritoneal macrophages (adherence to tissues, mobility directed to a chemical gradient from an infectious focus or chemotaxis, phagocytosis of foreign agents and destruction of these agents by superoxide anion production) and in lymphocytes (adherence and chemotaxis) from peritoneum, axillary lymph nodes, spleen and thymus. We used young (12 weeks), adult (22 weeks), mature (48 weeks) and old (72 weeks) female BALB/c mice. The adherence capacity of macrophages and lymphocytes was greater in adult and old mice than in young animals. The chemotaxis of macrophages showed higher values in cells from young mice than in those from adult mice, increasing again in macrophages from mature and old animals. A similar behaviour was shown by phagocytosis, which reached its highest values in old animals. Anion superoxide production increased with age and again the highest values were obtained in the oldest mice. Conversely, chemotaxis of lymphocytes was higher in the adult and mature animals than in the young and old animals. We conclude that, although there is a decrease in lymphocyte chemotaxis in old animals, the non-specific immune response of macrophages instead of decreasing, may increase in aged mice with respect to the values seen in adult mice.
Experimental Physiology 10/2000; 85(5):519-25. · 3.21 Impact Factor
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ABSTRACT: Exercise modulates the macrophage activity via 'stress hormones'. Three experiments were performed. (1) The effect of strenuous exercise performed by trained mice on macrophage chemotactic capacity was evaluated; (2) peritoneal macrophages from control mice were incubated with plasma from exercised mice or control mice and the differences in chemotaxis were measured; (3) changes in plasma T3 and T4 levels after exercise were measured, and the effect of incubation with the post-exercise levels of plasma T3 and T4 on chemotaxis was then studied in vitro. A 10(4)-fold higher concentration of each hormone was also evaluated. Exercise provoked an increase in chemotaxis (104 +/- 35 vs. 47 +/- 11 in controls). Incubation with plasma from exercised mice led to an increased level of chemotaxis. Incubation with concentrations of T3 and T4 similar to those observed in post-exercise plasma (T3, 2.3 nmol l(-1); T4, 84 nmol l(-1)) enhanced chemotaxis with respect to incubation with the basal concentrations of the hormones in control animals. A 10(4)-fold concentration of T4 reversed this effect. It is concluded that thyroid hormones stimulate macrophage chemotaxis. Also, these data support the hypothesis that thyroid hormones may be involved in exercise-induced stimulation of chemotaxis.
Molecular and Cellular Biochemistry 12/1999; 201(1-2):41-7. · 2.06 Impact Factor
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ABSTRACT: It is well known that a bidirectional relation exists between the immune and the classic animal regulation systems, the nervous and endocrine systems. It has also been reported that ageing has a negative effect on neuro-immuno-endocrine integration. Since it has been shown that norepinephrine (NE) differently modulates the phagocytic process of macrophages from young or old mice, and considering that NE has a short lifetime, the aim of this study is to evaluate the possible immunomodulatory role of the NE end-metabolite, 4-hydroxy-3-methoxyphenyl-glycol (HMP-glycol), on the superoxide anion levels of peritoneal macrophages from young-adult (22+/-2 weeks) and old (72+/-2 weeks) BALB/c mice. Macrophages were incubated with HMP-glycol in a range of concentrations between 10(-12) and 10(-3)M, and superoxide anion levels (both extracellular and intracellular) were evaluated by using the NBT reduction test. The response of macrophages to HMP-glycol was different between young-adult and old animals. While all concentrations (10(-12), 10(-9), 10(-7), 10(-5), 10(-3)M) of HMP-glycol led to lower extracellular O(-)(2) levels (p<0.05) in macrophages from young-adult mice, only the 10(-3)M concentration of HMP-glycol led to a significant decrease in the extracellular O(-)(2) production in macrophages from old mice. No significant changes were found in the intracellular O(2)(-) levels when macrophages were incubated with the different concentrations of HMP-glycol in either young-adult or old mice. Thus, the modulation of macrophage function by NE not only depends on their concentration, but also on the products of NE catabolism. The effect of NE metabolite will also depend on the age of the animals as there is an age-dependent decreased capacity to respond to low concentrations of HMP-glycol.
Experimental Gerontology 37(2-3):395-400. · 3.74 Impact Factor
