Immunity plays an important role in the reactivity of the organism and, in this context, is an essential factor in the pathogenesis of many diseases. Basically, there is no system or organ in the body, whose dysfunction is not related to immunity consequences. In addition, there are also multisystem diseases simultaneously involving multiple body systems. They are not always caused by weak immunity, but also often by modified immune reactions known as overshooting. The essence of all these diseases is a change in the reactivity of the organism where immunity plays an important role. The immunity as such is then part of the systems of neuroendocrine-immune regulation, which have common mediators and receptors. The establishment of psychoneuroimmunology, a relatively new discipline in neuroscience, contributed to a detailed understanding of these mechanisms between central and peripheral nervous system, the endocrine system and the immune system. This research enabled the uncovering of the nature of stress-diseases and impact of other regulatory disturbances on the function of various body organs and systems of the organism as a whole. The aim of this short review is to show complex interconnections of these relationships to better understand the human health and disease., F. Vožeh., and Seznam literatury
Atherosclerosis is a degenerative inflammatory disease of the vascular wall, which is characterized by the formation of atherosclerotic plaques that contain lipids, activated smooth muscle cells, immune cells, foam cells, a necrotic core and calcified sites. In atherosclerosis pathology, monocytes and macrophages play the most important role by accumulating redundant LDL particles in their oxidized form and producing proinflammatory cytokines. Atherosclerotic plaque macrophages reveal distinct phenotypes that are distinguished into M1 (proinflammatory) and M2 (anti-inflammatory) macrophages. Numerous environmental signals (cytokines, microbial cell molecules) that are received by macrophages drive their polarization, but it must be determined whether this classification reflects different macrophage subtypes or plasticity and phenotypic tissue changes, but the balance between subsets is crucial. M1 macrophages are dominant in symptomatic atherosclerotic plaques, while M2 macrophages are more frequent in asymptomatic plaques. Nevertheless, a positive correlation of both M1 and M2 macrophages with atherosclerotic lesion severity was also observed., A. Králová, I. Králová lesná, R. Poledne., and Obsahuje bibliografii
Immunomodulatory steroids, dehydroepiandrosterone and its 7-hydroxylated metabolites and sex hormone-binding globulin (SHBG) were determined in sera of 88 women aged 18-75 years. The group consisted of 34 healthy women, 37 women with subclinical and 17 women with manifest hypothyroidism. In all subjects the laboratory parameters of thyroid function (thyrotropin, free thyroxine and triiodothyronine) and thyroid autoantibodies to thyroid peroxidase and thyroglobulin were determined. The aim was to find out 1) whether the above steroids and SHBG levels differ in individual groups according to thyroid status, 2) whether correlations exist among investigated steroids and thyroid laboratory parameters, and 3) whether the respective steroid and SHBG levels differ according to the presence of principal thyroid autoantibodies. With the exception of 7β-hydroxy-dehydroepindrosterone levels, which were decreased in patients with manifest hypothyroidism (p<0.05), no significant differences in steroid and SHBG levels among groups according to diagnosis were found. On the other hand, significantly decreased levels of all the immunomodulatory steroids studied were found in subjects with positive titres of thyroid autoantibodies. This finding was supported by a tight negative correlation among the above steroids and thyroid autoantibodies. In addition, these steroids correlated negatively with thyrotropin and positively with free thyroid hormones. The results point to a negative relationship between the above mentioned immunoprotective steroids and the extent of the autoimmune process in hypothyroidism., K. Drbalová, P. Matucha, M. Matějková-Běhanová, R. Bílek, L. Kříž, H. Kazihnitková, R. Hampl., and Obsahuje bibliografii a bibliografické odkazy
No data are available about the effects of AT1 receptor antagonist losartan on the skeleton and there is also little information on the activity of an ACE inhibitor enalapril on bone metabolism. It is widely believed that the vasculature plays an important role in bone remodeling under normal and pathological conditions. We treated 14-week-old female Wistar rats with losartan, enalapril or saline. Administration of the ACE inhibitor enalapril and angiotensin II antagonist losartan had no effect on total malondialdehyde (MDA) in the blood and on urinary excretion of some eicosanoids and their metabolites. The administration of enalapril and losartan in a dose recommended for the treatment of hypertension did not cause significant changes in bone density, the ash and mineral content or morphometric parameters of the femur compared to the values found in control female rats., P. D. Broulík, V. Tesař, T. Zima, M. Jirsa., and Obsahuje bibliografii
The normal retinal development is interrupted by preterm birth and a retinopathy of prematurity (ROP) may develop as its consequence. ROP is characterised by aberrant vessel formation in the retina as a response to multiple risk factors influencing the process of retinal angiogenesis. Insulin-like growth factor I (IGF -1) and vascular endothelial growth factor (VEGF) play an important role in the process of normal retinal vascularisation. Insufficient nutrition during the first 4 postnatal weeks results in low serum levels of IGF-1, which is essential for correct retinal vessels formation, ensuring survival of the newly formed endothelial cells. Low IGF-1 level results in stop of angiogenesis in the retina, leaving it avascular and prompting the onset of ROP. Keeping the newborns in a positive energetic balance by providing enough nutrients and energy has a beneficial impact on their growth, neurodevelopment and decreased incidence of ROP. The best way to achieve this is the early parenteral nutrition with the high content of nutrients combined with early enteral feeding by the own mother's breast milk. Multiple studies confirmed the safety and efficacy of early aggressive nutrition but information about its long-term effects on the metabolism, growth and development is stil needed., N. Lenhartova, K. Matasova, Z. Lasabova, K. Javorka, A. Calkovska., and Obsahuje bibliografii
The impact of high -intensity exercise on disease progression and muscle contractile properties in experimental autoimmune encephalomyelitis (EAE) remains unclear. Control (CON) and EAE rats were divided into sedentary and exercise groups. Before onset (experiment 1, n=40) and after hindquarter paralysis (experiment 2, n=40), isokinetic foot extensor strength, cross sectional area (CSA) of tibialis anterior (TA), extensor digitorum longus (EDL) and soleus (SOL) and brain -derived neurotrophic factor (BDNF) levels were assessed. EAE reduced muscle fiber CSA of TA, EDL and SOL. In general, exercise was not able to affect CSA, whereas it delayed hindquarter paralysis peak. CON muscle work peaked and declined, while it r emained stable in EAE. BDNF -responses were not affected by EAE or exercise. In conclusion, EAE affected CSA -properties of TA, EDL and SOL, which could, partly, explain the absence of peak work during isokinetic muscle performance in EAE -animals. However, exercise was not able to prevent muscle fiber atrophy., I. Wens, U. Dalgas, K. Verboven, L. Kosten, A. Stevens, N. Hens, B. O. Eijnde., and Obsahuje bibliografii
The presence of insulin resistance is frequently found in essential hypertension. There are, however, only sparse data with respect to the potential presence of insulin resistance in patients with secondary hypertension. We have therefore undertaken a study to reveal the potential occurrence of insulin resistance in primary hyperaldosteronism (PH). The hyperinsulinemic euglycemic clamp technique together with the evaluation of insulin receptor characteristics were used to study insulin resistance in 12 patients with PH. The measured parameters were compared to normal values in control subjects. We have found a significantly lower glucose disposal rate (M, m mol/kg/min) (18.7± 6 vs. 29.3± 4), decreased tissue insulin sensitivity index (M/I, m mol/kg/min per mU/l x100) (23.7± 9.8 vs. 37.5± 11.6) and also lower metabolic clearance rate of glucose (MCRg, ml/kg/min) (3.8± 1.5 vs. 7.0± 1.1) in patients with primary hyperaldosteronism. The insulin receptor characteristics on erythrocytes did not differ in primary hyperaldosteronism as compared to control healthy subjects. We thus conclude that insulin resistance is also present in secondary forms of hypertension (primary hyperaldosteronism) which indicates the heterogeneity of impaired insulin action in patients with arterial hypertension., J. Widimský Jr., G. Šindelka, T. Haas, M. Prázný, J. Hilgertová, J. Škrha., and Obsahuje bibliografii
The aim of the study was to evaluate skin microvascular reactivity (MVR) and possible influencing factors (fibrinolysis, oxidative stress, and endothelial function) in patients with Cushing’s syndrome. Twenty-nine patients with active Cushing’s syndrome (ten of them also examined after a successful operation) and 16 control subjects were studied. Skin MVR was measured by laser Doppler flowmetry during post-occlusive (PORH) and thermal hyperemia (TH). Malondialdehyde and Cu,Zn-superoxide dismutase were used as markers of oxidative stress. Fibrinolysis was estimated by tissue plasminogen activator (tPA) and its inhibitor (PAI-1). N-acetyl-β-glucosaminidase, E-selectin, P-selectin, and ICAM-1 were used as markers of endothelial function. Oxidative stress and endothelial dysfunction was present in patients with hypercortisolism, however, increased concentration of ICAM-1 was also found in patients after the operation as compared to controls (290.8±74.2 vs. 210.9±56.3 ng.ml-1, p<0.05). Maximal perfusion was significantly lower in patients with arterial hypertension during PORH and TH (36.3±13.0 vs. 63.3±32.4 PU, p<0.01, and 90.4±36.6 vs. 159.2±95.3 PU, p<0.05, respectively ) and similarly the velocity of perfusion increase during PORH and TH was lower (3.2±1.5 vs. 5.2±3.4 PU.s-1, p<0.05, and 0.95±0.6 vs. 1.8±1.1 PU.s-1, p<0.05, respectively). The most pronounced impairment of microvascular reactivity was present in patients with combination of arterial hypertension and diabetes mellitus., M. Prázný, J. Ježková, E. Horová, V. Lazárová, V. Hána, J. Kvasnička, L. Pecen, J. Marek, J. Škrha, M. Kršek., and Obsahuje bibliografii a bibliografické odkazy
The aim of the study was to evaluate the impact of simulated acute hyperglycemia (HG) on PI3K/Akt signaling in preconditioned and non -preconditioned isolated rat hearts perfused with Krebs -Henseleit solution containing normal (11 mmol/l) or elevated (22 mmol/l) glucose subjected to ischemia -reperfusion. Ischemic preconditioning (IP) was induced by two 5 -min cycle s of coronary occlusion followed by 5 -min reperfusion. Protein levels of Akt, phosphorylated (activated) Akt (P-Akt), as well as contents of BAX protein were assayed (Western blotting) in cytosolic fraction of myocardial tissue samples taken prior to and a fter 30 -min global ischemia and 40- min reperfusion. In “normoglycemic ” conditions (NG), IP significantly increased P -Akt at the end of long -term ischemia, while reperfusion led to its decrease together with the decline of BAX levels as compared to non- pre conditioned hearts. On the contrary, under HG conditions, P -Akt tended to decline in IP - hearts after long -term ischemia, and it was significantly higher after reperfusion than in non -preconditioned controls . No significant influence of IP on BAX levels at the end of I/R was observed under HG conditions . It seems that high glucose may influence IP -induced activation of Akt and its downstream targets, as well as maintain persistent Akt activity that may be detrimental for the heart under above conditions., M. Zálešák, P. Blažíček, I. Gablovský, V. Ledvényiová, M. Barteková, A. Ziegelhöffer, T. Ravingerová., and Obsahuje bibliografii
We investigated and evaluated post-irradiation survival in cyclooxygenase-2-deficient (COX-2 KO) mice. Thirty-day survival following exposure of COX-2 KO mice to a lethal dose of 8.5 Gy of γ-rays was observed to be statistically significantly lower in both males and females, as well as when the sexes were merged, in comparisons with their wild-type counterparts. These findings were related to the previous observations concerning the detrimental influence of the COX-2 genetic disruption on hematopoiesis in sublethally irradiated mice. Deteriorated postirradiation survival of COX-2 KO mice confirmed the previously anticipated conclusion regarding negative influence of the antiinflammatory action of COX-2 deficiency under the conditions of exposure of the animals to ionizing radiation., M. Hofer, Z. Hoferová, A. Gruzdev, L. Dušek, M. Falk., and Obsahuje bibliografii