Biomedical subjects

N Reinisch

Publications and source records attributed to N Reinisch.

42 records · Page 3Linked to original sources

PubMed1993

Induction of normal human eosinophil migration in vitro by substance P.

To investigate the role of tachykinins in allergic inflammation, the effect of substance P (SP) on normal human eosinophil migration was examined in Boyden chamber type assays. SP stimulated eosinophil migration in vitro with an EC50 of about 1-10 pM and maximal effects were seen at 100 pM. A carboxy-terminal fragment of SP possessed appreciable activity whereas an amino-terminal fragment was inactive. Data represented in this paper and previous studies suggest that eosinophils are attracted by SP and activated to enhanced mediator release and cytotoxic activity.

Chemotaxis, Leukocyte↗

PubMed1992

In vivo activation of circulating monocytes by exogenous growth hormone in man.

Animal studies have shown that administration of growth hormone improves wound healing. Monocyte activation is a prerequisite for optimal repair of damage. In vitro, human recombinant growth hormone was shown to be a potent human monocyte chemoattractant. It induced random migration and chemotaxis at picomolar concentrations of recombinant human growth hormone; combinations of growth hormone with other chemoattractants deactivated the chemotactic response. Other functions of monocytes that are activated by growth hormone include release of superoxide anion and production of cytokines. In order to test activation of human monocytes by growth hormone in vivo, we investigated the effects of recombinant human growth hormone administration on monocyte migration in nine healthy young adults. After a single dose of recombinant human growth hormone (4 IU subcutaneously injected), random migration of circulating monocytes significantly increased, whereas chemotaxis of monocytes that was maximally stimulated with f-Meth-Leu-Phe decreased (p < .05). The alterations paralleled the concomitantly measured plasma levels of growth hormone. After recombinant human growth hormone administration, no changes were seen in plasma levels of proinflammatory cytokines. These in vivo data on monocyte migration are comparable to effects of growth hormone on monocyte migration in vitro and strongly suggest that recombinant human growth hormone can activate circulating monocytes in man.

Adult↗

PubMed1992

Proinflammatory cytokines in cardiac myxomas.

Serum levels of various cytokines were measured in three patients with cardiac myxomas presenting with and without constitutional symptoms, immunological features and elevated plasma levels of interleukin-6. Interleukin-6 but not other cytokines (interleukin-1, tumour necrosis factor-alpha, interferon-gamma) relate to immunological features of the patients. Circulating levels of atrial natriuretic peptide correspond to haemodynamic changes but not to the tumour-bearing state itself.

Atrial Natriuretic Factor↗

PubMedDate not supplied

Superoxide anion release from neutrophils in growth hormone deficient adults before and after replacement therapy with recombinant human growth hormone.

The observations that growth hormone primes neutrophils and stimulates various activities of monocytes suggested that it plays a role in the regulation of leukocyte biology. The in vivo reduction of growth hormone levels may be responsible for to the functional impairment of leukocytes observed in growth hormone deficient children. Whether leukocyte function is impaired in growth hormone deficient adults is not known as yet. We therefore studied superoxide anion release from neutrophils and chemotaxis of monocytes in 15 patients with adult-onset growth hormone deficiency before and after a period of 6 months of replacement therapy with recombinant human growth hormone. Analyses were performed by comparing functions of the leukocytes from these patients with those from age and sex-matched healthy control subjects. Before growth hormone treatment, patients received appropriate replacement therapy with thyroid, adrenal and gonadal hormones. The dose of recombinant human growth hormone was 0.25-0.5 U/kg/week (0.013-0.026 mg/kg/day) throughout the whole period of replacement therapy. In growth hormone deficient subjects, formylpeptide-triggered release of superoxide anions from neutrophils was significantly suppressed by about 40% before treatment as compared to healthy control subjects. After 6 months of replacement therapy, neutrophil superoxide anion release was similar in patients and healthy individuals. Neither before nor after replacement therapy, however, was there a difference in monocyte migration between control and growth hormone deficient subjects. These data indicate that neutrophil function is somehow altered in growth hormone deficient patients, even when receiving appropriate therapy with thyroid, adrenal and gonadal hormones, but that neutrophil function can be restored to near normalcy by growth hormone replacement therapy. This would suggest that suppressed neutrophil respiratory burst is due to the deficiency in growth hormone.

Adult↗

PubMedDate not supplied

Regulation of myeloid phagocyte development and function by growth hormone: a review.

Growth hormone (GH) has previously been implicated in T cell development and function, and here we review its efficacy in promoting development and function of myeloid cells. Evidence obtained from both in vitro and in vivo studies suggests that, in animals as well as in man, GH augments proliferation and differentiation of erythroid, megakaryocytic and myeloid progenitor cells. Mechanisms of hemopoietic actions probably involve induction of insulin-like growth factor-1, which is under GH control. Effects are mostly, though not exclusively, seen in GH deficiency states. Like other hemopoietic factors currently undergoing clinical trials for modulation of mature phagocyte function, GH is found in vitro and in vivo to stimulate potently monocyte migration and to prime neutrophils and macrophages for enhanced activation by second stimuli. Activation of neutrophils is mediated by GH action on the neutrophil prolactin receptors. The detailed mechanism of macrophage activation is currently unknown. GH action on myeloid phagocytes may help to explain protective effects of GH observed in experimental infection as well as its promotive effect on wound healing.

Animals↗

PubMedDate not supplied

Decrease of respiratory burst in neutrophils of patients with ankylosing spondylitis by combined radon-hyperthermia treatment.

OBJECTIVE: To define the respiratory burst activity of neutrophils, the total anti-oxidative status of plasma, and the parameters of systemic inflammation in patients with ankylosing spondylitis (AS) before and after a combined radon-hyperthermia treatment in the thermal tunnels of Böckstein-Bad Gastein in Austria. METHODS: In 20 patients with AS the effects of a total of 15 hours of radon-hyperthermia-treatment spread over a period of three weeks were studied. The respiratory burst activity of neutrophils was measured fluorometrically using dichlorofluorescein diacetate, the total anti-oxidant status was measured using azinodiethyl-benzthiazoline-sulphonate, and inflammation parameters were determined by routine laboratory assays. RESULTS: Before treatment, the basal neutrophil respiratory burst in patients (n = 20) was 409 +/- 62 fluorescence arbitrary units (AU; mean +/- SEM) and 359 +/- 37 AU in controls (n = 9; p > 0.5); the stimulated respiratory burst (fMet-Leu-Phe, 10(-6) M) was 1,027 +/- 133 AU in patients and 1,152 +/- 218 AU in controls (p > 0.5). After treatment, the basal neutrophil respiratory burst in patients (n = 19) was 137 +/- 16 and in controls it was 174 +/- 35 AU (n = 8; p > 0.1); the stimulated respiratory burst was 670 +/- 66 and 1,305 +/- 82 AU, in patients and controls respectively (p < 0.001). No effects of treatment on the total anti-oxidant status of the plasma or on the parameters of inflammation were detected. CONCLUSION: Combined radon-hyperthermia treatment reduces the respiratory burst activity of the blood circulating neutrophils in patients with AS. If respiratory burst activity from the neutrophils plays a role in the pathophysiology of ankylosing spondylitis, the observed reduction may be related to the beneficial effects of radon-hyperthermia treatment.

Adult↗