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Biomedical subjects

B K Pedersen

Publications and source records attributed to B K Pedersen.

At least 145 records · Page 8Linked to original sources
PubMed1997

In vivo cell-mediated immunity and vaccination response following prolonged, intense exercise.

Epidemiological and experimental studies have shown increased frequency and severity of infections after intense, long-term exercise. This study examines whether an in vivo impairment of the cell-mediated immunity and antibody production can be demonstrated after intense, long-term exercise. Twenty-two male triathletes performed one-half an ironman (group A). Vaccinations with tetanus and diphtheritis toxoid and purified pneumococcal polysaccharide were given after the exercise. Furthermore, a skin test with seven different antigens was applied on the forearm. Antibody titers were measured before and 2 wk after the exercise. The skin test was read 48 h after the application. Eleven non-exercising triathletes (group B) and 22 moderately trained men (group C) were used as control groups. Group A revealed a significantly lower skin test response to the tetanus antigen than both groups B and C. In group A, a smaller cumulative response (sum of the diameters of indurations and number of positive skin test spots) was found than in both groups B and C. No differences in antibody titers were found among the three groups. Thus, the in vivo cell-mediated immunity was impaired in the first days after prolonged, high intensity exercise, whereas there was no impairment of the in vivo antibody production measured 2 wk after vaccination.

Adult↗
PubMed1997

Prolonged submaximal eccentric exercise is associated with increased levels of plasma IL-6.

To study the relationship between exercise-related muscle proteolysis and the cytokine response, a prolonged eccentric exercise model of one leg was used. Subjects performed two trials [a branched-chain amino acid (BCAA) supplementation and a control trial]. The release of amino acids from muscle during and after the eccentric exercise was decreased in the BCAA trial, suggesting a suppression of net muscle protein degradation. The plasma concentrations of interleukin (IL)-6 increased from 0.75 +/- 0.19 (preexercise) to 5.02 +/- 0.96 pg/ml (2 h postexercise) in the control trial and in the BCAA supplementation trial from 1.07 +/- 0.41 to 4.15 +/- 1.21 pg/ml. Eccentric exercise had no effect on the concentrations of neutrophils, lymphocytes, CD16+/CD56+, CD4+, CD8+, CD14+/CD38+, lymphocyte proliferative response, or cytotoxic activities. BCAA supplementation reduced the concentration of CD14+/CD38+ cells. This study shows that the concentration of IL-6 in plasma is increased after prolonged eccentric exercise and suggests that the cytokine response is independent of the muscle proteolysis that occur during exercise.

Adult↗
PubMed1997

Splenectomy impairs lymphocytosis during maximal exercise.

To evaluate the role of the spleen for the exercise-induced lymphocytosis, six splenectomized subjects and six matched control subjects cycled for 12 min at two submaximal work rates corresponding to 50 and 75% of their maximal work capacity, followed by a supramaximal intensity maintained until exhaustion (16 +/- 1 min; mean +/- SE). Venous blood samples were taken before, during, and 2 h after the maximal load. In both groups, the concentration of lymphocytes became elevated during exercise, but the increase from the level at rest was impaired in the splenectomized subjects compared with that of the controls (118 +/- 34 vs. 238 +/- 38%; P < 0.05). This was reflected in several lymphocyte subsets: cluster designation (CD) 3+ cells (pan T lymphocytes), 69 +/- 19 vs. 204 +/- 37%; CD8+ cells (T lymphocyte subset), 164 +/- 41 vs. 467 +/- 68%; CD16+ cells [natural killer (NK) cells], 291 +/- 88 vs. 870 +/- 177%; CD56+ cells (NK cells), 301 +/- 108 vs. 753 +/- 187%. Also, the specific NK cell lysis of target cells (NK cell activity) during exercise was lower for the splenectomized subjects (30 +/- 7%) than that of the control subjects (52 +/- 10%), but evaluation of lytic units indicates that this was due to a reduced number of NK cells in the assay rather than insufficient cell lysis. Plasma catecholamines reached the same level in the splenectomized subjects and control subjects, which was taken to reflect that the activity of the sympathetic nervous system was similar in the two groups of subjects. Thus the major finding of this study is that the spleen is important for lymphocytosis during exercise, accounting for two-thirds of the increase in T lymphocytes and NK cells.

Adult↗
PubMed1997

Adrenergic beta 1- and beta 1 + 2-receptor blockade suppress the natural killer cell response to head-up tilt in humans.

To evaluate stress-induced changes in blood leukocytes with emphasis on the natural killer (NK) cells, eight male volunteers were followed during three trials of head-up tilt with adrenergic beta 1- (metoprolol) and beta 1 + 2- (propranolol) blockade and with saline (control) infusions. The beta 1- and beta 1 + 2-receptor blockade did not affect the appearance of presyncopal symptoms, but the head-up tilt induced a transient lymphocytosis that was abolished by beta 1 + 2-receptor blockade but not by beta 1-receptor blockade. Head-up tilt also resulted in delayed neutrophilia, which was insensitive to beta-receptor blockade. Lymphocyte subset analysis revealed that the head-up tilt resulted in a twofold increase in the percentage and absolute number of CD3-/CD16+ and CD3-/CD56+ NK cells in peripheral blood and that this increase was partially blocked by metoprolol and abolished by propranolol. The NK cell activity on a per NK cell basis did not change during head-up tilt, indicating that the cytotoxic capability of NK cells recruited to circulation is unchanged. The data suggest that the head-up tilt-induced lymphocytosis was due mainly to CD16+ and CD56+ NK cells and that their recruitment to the blood was inhibited by beta 1- and especially beta 1 + 2-receptor blockade. Thus stress-induced recruitment of lymphocytes, and of NK cells in particular, is mediated by epinephrine through activation of beta-receptors on the lymphocytes.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1996

Mycobacterium avium and purified protein derivative-specific cytotoxicity mediated by CD4+ lymphocytes from healthy HIV-seropositive and-seronegative individuals.

HIV is the greatest single risk factor for the development of tuberculosis. Diseases caused by M. tuberculosis and mycobacteria are the most common opportunistic infections in HIV-infected persons, which may stem from a functional defect of the CD4+ T-cell-mediated killing of macrophages harboring mycobacteria. Our objective was to investigate the M.tuberculosis-and M. avium-specific cytotoxic capacity of T cells from healthy, bacille Calmette-Guérin-vaccinated, HIV-seropositive individuals. Blood mononuclear cells were obtained from 10 healthy HIV-seropositive and 10 healthy seronegative persons with no history of previous or active mycobacterial infection. Antigen-specific killing of macrophages presenting mycobacterial antigens (purified protein derivative or M. avium culture filtrate) was conducted. The phenotype of the killer cells was determined by a fluorescence-activated cell sorter after antigen stimulation and by using purified CD4+ and CD8+ cell subsets. Substantial, but reduced antigen-specific cytotoxicity was observed in patients with asymptomatic HIV infection. The immunological dysfunction leading to reduced cytotoxic activity in healthy HIV-seropositive subjects could not be explained by a defect in the cytotoxic capacity of the individual CD4+ lymphocyte after antigen stimulation, and it could not be explained by a reduction in the total number of CD4+ cells before antigen stimulation. The antigen-specific cytotoxic activity was, however, closely related to the ability of the CD4+ T cells to respond to mycobacterial antigens. The immunological dysfunction leading to reduced mycobacterial-specific cytotoxic activity in healthy HIV-seropositive subjects is caused either by a reduction in the number of antigen-responsive CD4+ T cells (memory) or by an impairment of their ability to respond to antigenic stimuli.

Adult↗
PubMed1996

[Primary HIV infection].

Up to 70% of individuals with primary HIV infection will develop symptoms of an acute illness. The most common symptoms reported are fever, generalized lymphadenopathy, arthralgia and myalgia, headache, pharyngitis, enanthema, skin rash, diarrhoea, and mucocutaneous ulcerations. More rarely, oesophageal candidiasis, meningoencephalitis, rhabdomyolysis and epiglottitis have been reported. The diagnosis of the acute HIV infection syndrome can be established by demonstrating antibodies to HIV or by demonstration of HIV antigen positivity. Detection of virus through culture or PCR may prove to be more sensitive, but are not yet used as routine methods. The course of the primary infection has prognostic importance for the subsequent course of HIV infection. This probably reflects the importance of both the viral phenotype and of the initial immune response to HIV. Primary HIV infection should be considered in any patient with possible exposure to HIV presenting with fever of unknown cause.

HIV Infections↗
PubMed1996

[Primary HIV infection. Case histories].

More than 50% of individuals with primary HIV infection have a symptomatic febrile illness associated with seroconversion. The most common clinical picture is a mononucleosis-like or influenza-like illness but almost any organ system may be involved, and primary HIV infection is often an imitator of other acute diseases. Six cases of symptomatic primary infection are described, one with a characteristic presentation, and five cases respectively presenting with colitis, rhabdomyolysis, epiglottitis, cold agglutination haemolysis and meningitis as marked symptoms.

Adult↗
PubMed1996

The immune system and serum glutamine during a triathlon.

This study examined the influence of a triathlon on the immune system and on serum amino acid concentrations. Eight male triathletes swam 2500 m, bicycled 81 km, and ran 19 km. The concentration of total serum amino acids decreased during the race, with the lowest values occurring 2 h postexercise. Similarly, serum glutamine concentration declined from 468 (SEM 24) (prerace) to 318 (SEM 20) mumol-1 (2 h postrace) and the natural killer (NK) and lymphokine activated killer (LAK) cell activities were suppressed 2 h postexercise (P < 0.05). Blood mononuclear cell proliferation decreased during exercise with the lowest value observed after running. The leucocyte concentration increased during and after exercise due to an increase in the concentration of neutrophils and monocytes. There was no significant change in lymphocyte concentration during or after the exercise. The plasma concentration of interleukin-6 did not change and the plasma concentration of interleukin-1 beta and tumor necrosis factor-alpha were below detection limits. The LAK cell cytotoxicity, but not NK cell activity or proliferative response, was significantly correlated with serum glutamine concentrations (r = 0.39, P < 0.01). This study confirms that prolonged endurance exercise results in changes in the cytotoxic function of the NK and LAK cells as well as the proliferative response. The time-course of changes in serum glutamine concentrations were best parallelled by changes in LAK cell activities.

Adult↗
PubMed1996

Lymphocyte, NK and LAK cell responses to maximal exercise.

To evaluate if exhaustion after maximal exercise suppresses the immune system; ten healthy male oarsmen (maximal oxygen uptake, 5.7 +/- 0.2 l.min-1; mean and SE) performed a six minute "all-out" bout on a rowing ergometer (394 +/- 12 watt). Rowing increased the blood leucocyte count as reflected in the concentrations of lymphocytes, monocytes, and neutrophils. Two hours after rowing the leucocyte and neutrophil numbers remained elevated, while the lymphocyte count decreased below the prevalue. The concentrations of cluster designation CD3+ (pan T), CD4+ (T subset), CD8+ (T subset), CD19+ (B cells), and CD16+ natural killer (NK) cells increased during rowing with the elevation in CD16+ cells being sevenfold. Only the concentration of CD3+ and CD8+ cells decreased below prevalues two hours after exercise. The lymphokine activated killer (LAK) cell activity of blood mononuclear cells (BMNC), and the NK cell activity of BMNC (%lysis per fixed number of BMNC), either unstimulated or stimulated with interleukin-2, interferon-alfa or indomethacin, also increased in response to rowing, and returned to the prevalues after two hours. In contrast, the BMNC proliferative responses did not change significantly. The evaluation of NK and LAK cell activities, and the proliferative responses of BMNC suggest that six minute maximal exercise does not suppress the immune response during recovery, even when a large muscle mass is involved.

Adult↗
PubMed1996

Lymphocytes and NK cell activity during repeated bouts of maximal exercise.

Effects on the immune system of 6-min "all-out" ergometer rowing were investigated over 2 days (2 x 3 bouts) in eight male oarsmen with a maximal oxygen uptake of 5.5 +/- 0.1 l/min (mean +/- SE). Blood samples were obtained before, during, and 2 h after each bout and on the day after the last bout. Compared with levels at rest, the first bout of exercise increased the concentration of leukocytes (2-fold); neutrophilic granulocytes (2-fold); lymphocytes (2-fold); monocytes (2-fold); the blood mononuclear cell (BMNC) subsets CD3+ (2-fold), CD4+ (2-fold), CD8+ (3-fold), CD16+ (8-fold), CD19+ (2-fold), and CD14+ (2-fold); the NK cell activity (2-fold); and plasma interleukin-6 (3-fold) (P < 0.05). During the last bout even higher levels were noted for leukocytes (3-fold); neutrophilic granulocytes (3-fold); lymphocytes (4-fold); the BMNC subsets CD4+ (3-fold), CD8+ (5-fold), CD16+ (13-fold), CD19+ (5-fold), and CD14+ (3-fold); and for the NK cell activity (4-fold) (P < 0.05). During the recovery periods all values were at or above the level at rest, and elevated concentrations of leukocytes (38%), neutrophilic granulocytes (48%), and lymphocytes (46%) reflected in the BMNC subsets and increased NK cell activity (119%) were also noted on the day after the last bout (P < 0.05). The results show that maximal exercise with large muscle groups provokes higher immune responses during repetitive bouts.

Adult↗
PubMed1996

Immunity in athletes.

It has become clear that the immune system responds to increased physical activity and may be given some of the credit for exercise-related reduction in illness. In contrast, it has repeatedly been shown that intense exercise causes immunosuppression. In essence the immune system is enhanced during moderate and severe exercise, and only intense long-duration exercise is followed by immunodepression. The latter include suppressed concentration of lymphocytes, suppressed natural killer and lymphokine activated killer cytotoxicity and secretory IgA in mucosa. Whether or not the "open window" in the immune system occurs is dependent on the intensity and duration of exercise. One reason for the "overtraining effect" seen in elite athletes could be that this window of opportunism for pathogens is longer and the degree of immunosuppression more pronounced. It is being hypothesized that severe immunodepression may occur if athletes does not allow the immune system to recover, but initiate a new bout of exercise while still immunodepressed. It has also been suggested that neutrophils serve as a last line of defence. The removal of this back-up system following extreme activity would be compatible with the propensity of "overtrained" individuals to develop upper respiratory tract infections.

Cytotoxicity, Immunologic↗
PubMed1995

Increase in percentage of CD45RO+/CD8+ cells is associated with previous severe primary HIV infection.

The purpose of the study was to examine how memory (CD45RO) and naive (CD45RA) phenotypes of CD4+ and CD8+ T-cell subpopulations changed with respect to progression and duration of human immunodeficiency virus (HIV) infection. Forty-three HIV-seropositive (HIV+) subjects with known time for seroconversion were included in this cross-sectional study. They were divided into the following groups for comparison: persons with and without AIDS, persons who had seroconverted > 72 and < 72 months before entering the study, persons with or without previous severe primary infection, persons who had developed AIDS > 72 and <72 months before entering the study. Furthermore, the HIV+ group was compared with an HIV-seronegative (HIV-) age- and sex-matched group. There was no difference in the proportion of total naive relative to total memory cells between HIV+ and HIV- subjects, showing an equal loss of naive and memory CD4+ cells in this study. Moreover, there was no difference in the proportion of total naive relative to memory CD8+ cells, showing an equal increase in both subgroups of CD8+ cells in HIV+ subjects. However, HIV+ subjects who had experienced severe primary symptoms resembled the AIDS group regarding shift in the CD8 phenotype from naive to memory and by down-regulation of amounts of CD45RA protein. Furthermore, the results showed that during infection with HIV the amounts of both CD45RA and CD45RO markers on CD4+ cells and CD45RA on CD8+ cells were down-regulated, although with different kinetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗