[Nurses' co-responsibility].
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Consumer Behavior↗
Biomedical subjects
B K Pedersen
Publications and source records attributed to B K Pedersen.
[Nursing care--cancer patients miss contact].
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Ambulatory Care↗
Levels of complement receptor type one (CR1, CD35) on erythrocytes, circulating immune complexes and complement C3 split products C3d and C3c are not changed by short-term physical exercise or training.
The effect of heavy short-term physical exercise on the levels of complement receptor type one (CR1, CD35) on erythrocytes, the concentrations of circulating immune complexes (IC), and the complement C3 split products C3c and C3d were examined in young healthy males. Fourteen untrained volunteers underwent a 60-min bicycle exercise test at 75% of maximal oxygen uptake (VO2max). Six of the volunteers were exercised twice with an interval of at least one month. Before the second bicycle test they received oral indomethacin. With an interval of at least 1 week, 6 also went through a 60-min back-muscle exercise at up to 30% of VO2max. Blood samples were collected before and during the last few minutes of exercise as well as 2 h and 24 h afterwards. The same parameters were examined once in 29 highly trained racing cyclists. There were no consistent or significant exercise-induced changes in the levels of erythrocyte CR1, circulating IC, C3c nor C3d as measured by an enzyme-linked immunosorbent assay, polyethylene glycol precipitation complement consumption method, and by intermediate gel rocket immunoelectrophoresis, respectively. Neither did these parameters differ from controls in the highly trained group. The results indicate that CR1 on erythrocytes, circulating immune complexes and complement cleavage products C3c and C3d in healthy subjects remain unaffected by short-term heavy physical activity and training.
Adult↗
Effect of physical exercise on in vitro production of interleukin 1, interleukin 6, tumour necrosis factor-alpha, interleukin 2 and interferon-gamma.
The present study was designed to examine the effect of physical exercise on production of interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2) and interferon-gamma (IFN-gamma). Ten young, healthy volunteers underwent 60-min bicycle exercise at 75% of maximal oxygen uptake (VO2max). Blood samples were collected before and during the last minutes of exercise, as well as 2 h and 24 h later. Blood mononuclear cells (BMNC) were stimulated in vitro with either bacterial lipopolysaccharide or phytohaemagglutinin, and the supernatants were tested for the above-mentioned cytokines using bioassays as well as ELISA techniques. The production of IL-6 increased significantly 2 h after exercise, furthermore the production of IL-1 alpha and IL-1 beta was enhanced, although only borderline significant. TNF-alpha, IL-2 and IFN-gamma did not fluctuate in relation to exercise. The increased amounts of IL-1 and IL-6 in the supernatants generated from a fixed number of BMNC are most likely explained by the increased percentage and absolute number of blood monocytes 2 h after exercise. IL-2 and IFN-gamma are mainly produced by CD4+ and CD16+ cells. During exercise the CD4+ subset decreases, while the CD16+ subset increases. The finding of unchanged production of IL-2 and IFN-gamma was therefore expected.
Adult↗
Influence of physical activity on the cellular immune system: mechanisms of action.
This review deals with the effect of acute physical exercise and training status on different components of the immune system. Predominantly studies in humans are mentioned. In relation to acute physical exercise (75% of VO2max, 1 hour) the leukocyte concentration increased; following exercise the neutrophils increased fourfold. The lymhphocyte concentration increased during and decreased following exercise. The percentage of CD3+ cells (pan T cells) declined during exercise, mainly due to a fall in the %CD4+ cells. The %CD16+ cells (NK cells) increased two-fold and returned to prevalue two hours after exercise. The %CD20+ cells (B cells) did not change in relation to exercise, whereas the %CD14+ cells (monocytes) increased two to threefold following exercise. The NK cell activity increased during but decreased following exercise. These increases were due to recruitment of NK cells with a high IL-2 response capacity, whereas the decreased NK activity post-exercise was due to downregulation by prostaglandins released by the elevated concentration of monocytes. During severe, moderate as well as light exercise, the NK cell activity increased, but the post-exercise suppression of the NK cell function was found only following severe exercise, and not after moderate or light exercise, furthermore, only following severe exercise, an increased monocyte concentration was demonstrated. The IL-2-stimulated lymphocyte proliferative response increased due to stimulation of CD16+ cells and did not reflect expression of IL-2 receptors.
Cytokines↗
Effects of in vivo hyperthermia on natural killer cell activity, in vitro proliferative responses and blood mononuclear cell subpopulations.
This work was designed to test the hypothesis that elevations in body temperature of humans induce immunostimulation. Eight healthy volunteers were immersed in a water bath (water temperature 39.5 degrees C) for 2 h, during which their rectal temperature rose to 39.5 degrees C. On a later day they served as their own controls, being immersed into thermoneutral water (34.5 degrees C) for 2 h. Blood samples were collected before immersion, at body temperatures of 38 degree C, 39 degree C and 39.5 degree C, and 2 h after water immersion. The interleukin-2 (IL-2) enhanced natural killer (NK) cell activity (lysis per fixed number of mononuclear cells), as well as the proportion and total number of NK cells (CD16+ cells), increased significantly during hyperthermia compared with control values. The lymphocyte proliferative responses did not differ significantly between hyperthermia and thermoneutral conditions. The proportion of pan-T (CD3+) cells was maximally depressed 2 h after water immersion. The decreased proportion of CD3+ cells was mainly due to a decreased percentage of CD4+ cells (not significant). The proportion of B cells (CD19+ cells) did not fluctuate significantly, while a marked and significant increase in monocyte proportion (CD14+ cells) was found 2 h after hyperthermia. Two hours after hot water immersion the lymphocyte concentration declined while the neutrophil and monocyte concentrations were augmented. Induced hyperthermia causes significantly increased serum cortisol, plasma norepinephrine and plasma epinephrine concentrations compared to controls. It is possible that the altered immune functions induced by elevated body temperature can be ascribed to altered composition and function of blood mononuclear cells induced by elevated levels of stress hormones.
Adult↗
Evidence that the effect of physical exercise on NK cell activity is mediated by epinephrine.
The present study was designed to test the hypothesis that the changes in natural killer (NK) cell activity in response to physical exercise were mediated by increased epinephrine concentrations. Eight healthy volunteers 1) exercised on a bicycle ergometer (60 min, 75% of maximal O2 uptake) and 2) on a later day were given epinephrine as an intravenous infusion to obtain plasma epinephrine concentrations comparable with those seen during exercise. Blood samples were collected in the basal state, during the last minutes of exercise or epinephrine infusion, and 2 h later. The NK cell activity (lysis/fixed number of mononuclear cells) increased during exercise and epinephrine infusion and dropped below basal levels 2 h afterward. The increased NK cell activity during exercise and the epinephrine infusion resulted from an increased concentration of NK (CD16+) cells in the peripheral blood. On the other hand, the decreased NK cell activity demonstrated 2 h after exercise and epinephrine infusion did not simply reflect preferential removal of NK cells from the blood, because the proportion of CD16+ cells was normalized. On the basis of the finding that indomethacin abolished the suppressed NK cell activity in vitro and the demonstration of a twofold increase in the proportion of monocytes (CD14+ cells) 2 h after exercise and epinephrine infusion, we suggest that, after stress, prostaglandins released by monocytes are responsible for downregulation of NK cell function. Our findings support the hypothesis that increased plasma epinephrine during physical stress causes a redistribution of mononuclear subpopulations that results in altered function of NK cells.
Adult↗
The effect of prophylaxis with chloroquine and proguanil on delayed-type hypersensitivity and antibody production following vaccination with diphtheria, tetanus, polio, and pneumococcal vaccines.
In vitro studies have shown that anti-malarial drugs suppress immunity. In this study, the effects of chloroquine and proguanil (Paludrine) on the cellular and humoral immune system were measured by two in vivo methods: 1) cell-mediated immunity (delayed cutaneous hypersensitivity) i.e., skin tests with seven delayed-type common antigens (Multitest) and 2) humoral immunity by measurement of specific antibody response to vaccination. Sixty healthy young individuals were randomized into four groups and given 1) no treatment (controls), 2) chloroquine diphosphate (500 mg/week), 3) chloroquine diphosphate (1,000 mg/week), or 4) proguanil hydrochloride (200 mg/day) for six weeks. Skin testing was performed on days 0 and 28. Vaccinations with diphtheria, tetanus, polio, and pneumococcal polysaccharide antigen vaccines were performed on day 28, and the presence of specific antibodies was determined on days 0, 28, and 42. The skin tests induced a significant increase in skin reactive areas from day 0 to day 28 in all groups. Furthermore, the skin test induced an increase in the level of specific IgG for diphtheria and tetanus, but had no effect on antibodies to antigens not included in the skin test. The results showed that there were no significant differences among the four groups regarding skin test areas and increases in antibody titers following vaccination. Therefore, it is concluded that in healthy persons, six weeks intake of chloroquine, even in double doses, or proguanil in chemoprophylactic dosages, does not induce any detectable suppression of delayed-type hypersensitivity or vaccination responses to diphtheria, tetanus, polio, or pneumococcal polysaccharide antigens.
Adult↗
Effects of in vitro hyperthermia on the proliferative response of blood mononuclear cell subsets, and detection of interleukins 1 and 6, tumour necrosis factor-alpha and interferon-gamma.
The role of endogenously mediated fever and exogenous hyperthermia as modulators of immune functions remains poorly understood. It is known that fever is mediated by several cytokines, including interleukin-1 alpha and interleukin-1 beta (IL-1 alpha and IL-1 beta), interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and the interferons. The present communication examines the effect of exogenous hyperthermia on the detection of these cytokines and shows the suppressive effect of elevated temperature (39 degrees) on the amount of IL-1 beta, IL-6 and IFN-gamma (P less than 0.001) but not on IL-1 alpha and TNF-alpha concentrations. It is suggested that a negative feedback mechanism exists between temperature and the production of some of the molecules involved in the mediation of fever. It is known that hyperthermia increases the proliferative response of lymphocytes. We found a twofold increase in [3H]thymidine incorporation at 39 degrees compared to 37 degrees. The distribution of cells expressing CD3, CD4, CD8, CD14, CD16, CD19 and CD25 markers was the same at 37 degrees and 39 degrees.
Antigens, CD↗
Immune parameters in male atheletes after a lacto-ovo vegetarian diet and a mixed Western diet.
The influence of a lacto-ovo vegetarian diet versus a meat-rich Western diet on in vitro measures of immune function was studied in eight male endurance athletes. Subjects consumed two different diets for 2 x 6 wk, separated by 4 wk on an ad libitum diet, in a cross-over design. Both diets consisted of 57 energy % (E%) carbohydrates, 14 E% protein and 29 E% fat. One diet was a mixed meat-rich diet (M) prepared with 69% animal protein sources, whereas the other diet (V) was a lacto-ovo vegetarian diet prepared with 82% vegetable protein sources. Blood for determination of leukocyte subpopulations and in vitro function was collected at the end of each diet period 36 h after the last training bout. Fiber content and P/S ratio of fatty acids were twice as high on the V diet as on the M diet. Training volume was similar on the two diets, and maximal aerobic capacity did not change during diet periods. The number of CD3+ (pan T-cells), CD8+ (mainly T suppressor cells), CD4+ (mainly T helper cells), CD16+ (natural killer cells), and CD14+ (monocytes) was similar after the two different diets. Similarly, proliferations of mononuclear cells after stimulation with interleukin-2 (IL-2), phytohemagglutinin, and purified derivative of tuberculin (PPD), as well as activity of natural killer cells in the unstimulated state and after stimulation with IL-2, indomethacin, and interferon-alpha (IFN-alpha), were identical after the two diet periods.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effects of isoprinosine treatment of HIV-positive patients on blood mononuclear cell subsets, NK- and T-cell function, tumour necrosis factor, and interleukins 1, 2, and 6.
The immunomodulatory drug isoprinosine has been found to delay the occurrence of opportunistic infections in HIV-infected individuals. To elucidate the mechanism of action, eight HIV-positive, healthy patients were treated with isoprinosine, 3 g/day for 28 days; six patients received no treatment but were examined in parallel, and two patients were withdrawn. All patients had blood collected just before the start as well as on days 14 and 28 of isoprinosine treatment. Isoprinosine significantly enhanced the lymphoproliferative response after stimulation with phytohaemagglutinin (PHA) and purified derivative of tuberculin (PPD), while isoprinosine had no effect on the following immune parameters: the expression of surface markers on blood mononuclear cells including CD2, CD3, CD4, CD8, CD14, CD19, CD20, CD25, leu-8, and HLA-DR. Furthermore isoprinosine did not influence the ability of interleukin 2 (IL-2) to stimulate the proliferation of lymphocytes or the natural killer (NK) cell activity either unstimulated or stimulated in vitro with alpha interferon (IFN-alpha), IL-2, or indomethacin. Neither did isoprinosine affect the in vitro production of (IL-1) alpha or beta, IL-2, IL-6, or tumour necrosis factor (TNF).
Adult↗
Methylprednisolone pulse therapy in acute severe asthma. A randomized, double-blind study.
Methylprednisolone pulse therapy (MPPT) has been shown to possess a long-lasting effect in other immune-inflammatory diseases without the well-known side effects caused by long-term treatment with glucocorticosteroids. In an attempt to reduce the long-term use of oral steroids in asthmatics, we conducted this double-blind, double-dummy study to compare the use of MPPT (1 g of methylprednisolone intravenously) (8 patients) with a short course of oral prednisolone (10 patients) in asthmatics presenting with acute severe asthma. Both treatments were effective in relieving the acute attack of asthma. The MPPT-treated patients did not show a faster resolution than did the orally treated group. No patients needed assisted ventilation, and no deaths occurred. One week after the treatment FEV1 tended to decrease in the methylprednisolone group compared with the oral prednisolone group (P = 0.06). The patients initially receiving MPPT needed supplementary prednisolone earlier and in higher doses than did the patients receiving oral prednisolone as initial treatment. At the end of the 12 weeks' study period, the groups reached identical FEV1. In conclusion, we did not find intravenous methylprednisolone superior to oral prednisolone in the treatment of acute attacks of severe asthma, but methylprednisolone pulse therapy had a shorter duration as regards protection against future asthma attacks.
Acute Disease↗
Natural killer cell functions are related to the cell membrane composition of essential fatty acids: differences in healthy persons and patients with primary Sjögren's syndrome.
To examine whether abnormalities in essential fatty acid (EFA) metabolism are associated with the impaired natural killer (NK) cell functions in primary Sjögren's syndrome, we measured the levels of phospholipid fatty acids in blood mononuclear cells with (MD) and without monocyte depletion (MC), and NK cell activity before and after indomethacin-boosting. We found MD levels of 20:3n6 (dihommo-gamma-linolenic acid), and basal and indomethacin-enhanced NK cell activity significantly reduced, in 10 primary Sjögren's syndrome patients as compared with 10 healthy controls. In the controls the relative (%) increase in indomethacin-enhanced NK cell activity correlated with the level of MD 18:2n6 (linoleic acid) (r = 0.97, p less than 0.001). In the patients the relative (%) indomethacin-enhanced NK cell activity correlated with the 20:4n6 (arachidonic acid)/20:3n6 ratio in the MC (r = 0.90, p less than 0.001). This ratio has been assumed to be an important determinant for the production of prostaglandin 1 and 2. The present data suggest that in healthy persons, as opposed to primary Sjögren's syndrome patients, the level of MD 18:2n6 is a determinant for the sensitivity of NK cells to monocyte-derived prostaglandins. Furthermore, in patients with primary Sjögren's syndrome the MC levels of 20:3n6 and 20:4n6 may be regulating factors for the production of NK cell suppressing prostaglandins.
Adult↗