Decreased chemotaxis of neutrophils in acromegaly and hyperprolactinemia

Mc, Fornari; Mf, Palacios; Ra, Díez; Ad, Intebi

doi:10.1530/eje.0.1300463

Cited by 18 publications

(9 citation statements)

References 23 publications

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“…Chemotaxis of neutrophils towards N-formylmethionyl-phenylalanine was significantly reduced in prolactinoma. Spontaneous migration was also reduced [31].…”

Section: Prolactinomamentioning

confidence: 94%

“…In contrast, chemotaxis of neutrophils towards N-formylmethionylphenylalanine was significantly reduced in acromegaly. Spontaneous migration was also reduced [30,31]. Although none of these changes led to abnormal defence against infectious diseases or autoimmunity, it has been suggested that the increase in cancer incidence was due to reduced immunosurveillance.…”

Section: Children With Gh Insensitivitymentioning

confidence: 99%

“…Several authors have studied NK function in hyperprolactinaemic patients [30][31][32][33][34][35]. In some studies the numbers of large granular lymphocytes and of CD56 + cells are reduced in women with puerperal hyperprolactinaemia or with prolactinoma [31,32] compared with normal controls. The reduction of NK activity was not seen if adherent cells had been removed [33].…”

Section: Prolactinomamentioning

confidence: 99%

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Prolactin, growth hormone and the immune system in humans

Velkeniers¹,

Dogusan²,

Naessens³

et al. 1998

CMLS, Cell. Mol. Life Sci.

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Prolactin (PRL) and growth hormone (GH) qualify as lymphoid growth and differentiation factors. Yet, long-standing hyper- or hyposecretion of PRL or GH does not induce any significant alteration of the immune system. Subclinical changes in laboratory parameters (such as chemotaxis or phagocytosis by granulocytes or macrophages or natural killer cell activity) have been reported in some of these conditions. The GH-insulin-like growth factor (IGF)-I axis is dysregulated in ageing, in catabolic states and in critical illness. Immune parameters, such as infection rate, are being monitored during clinical trials with GH or IGF-I. Hyperprolactinaemia may play an aggravating role in systemic lupus erythematosus, in autoimmune thyroiditis and in other autoimmune diseases. The patient may benefit from increased alertness about interactions between the endocrine and immune systems.

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“…Chemotaxis of neutrophils towards N-formylmethionyl-phenylalanine was significantly reduced in prolactinoma. Spontaneous migration was also reduced [31].…”

Section: Prolactinomamentioning

confidence: 94%

Section: Children With Gh Insensitivitymentioning

confidence: 99%

Section: Prolactinomamentioning

confidence: 99%

See 1 more Smart Citation

Prolactin, growth hormone and the immune system in humans

Velkeniers¹,

Dogusan²,

Naessens³

et al. 1998

CMLS, Cell. Mol. Life Sci.

View full text Add to dashboard Cite

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“…PRL reduces direct and spontaneous migration (469) of polymorphonuclear cells (469), regulates lymphocyte-epithelial cell adhesive interactions in the thymic nurse cell complex (470), and augments IgA-secreting plasma cells in mammary gland (471).…”

Section: F Immunoregulation and Protectionmentioning

confidence: 99%

Prolactin (PRL) and Its Receptor: Actions, Signal Transduction Pathways and Phenotypes Observed in PRL Receptor Knockout Mice

1998

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“…However, GH deficient individuals demonstrate an increased mortality from cardiovascular and respiratory causes [93], and neutrophils isolated from patients with acromegaly (excess GH) or hyperprolactinemia show decreases in directed (fMLP) and spontaneous chemotaxis [94]. Somewhat paradoxically, neutrophil phagocytic function and the generation of superoxide is reduced in patients with growth hormone deficiency (GHD) syndrome, and growth hormone replacement therapy [95][96][97] normalizes these functions.…”

Section: Growth Hormone Insulin-like Growth Factor and Somatostatinmentioning

confidence: 99%

Modulation of Neutrophil Function by Hormones

Mathison

2006

CIR

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Endocrine regulation of the neutrophilic component of innate immunity with a particular focus on the production of reactive oxygen species (ROS) is the subject of this review. Endocrine hormones contribute to neutrophil mediated pathology in several ways either by directly activating the cells, as is the case with an angiotensin activation of NADPH oxidase on neutrophils and monocytes to contribute to atherosclerosis, or by having biphasic effects depending upon the stage of systemic inflammation, i.e. in a hyper-inflammatory phase or a hypo-inflammatory or anergic state, as seen with growth hormone. Some factors, such as a novel anti-inflammatory peptide from salivary glands, the tripeptide FEG, and hypothalamic proline-rich peptide have more subtle effects and appear to negatively regulate the priming events required for neutrophil activation. Investigations on the impact and role of endocrine hormones on neutrophil function and ROS production have contributed to the understanding of the efficacy of some medications in treating inflammation, as is the case with the angiotensin receptor blockers, and should lead to the development of novel drugs that modulate innate immune system function and the severity of an inflammatory response.With the exception of a small number of anaerobic bacteria oxidation reactions are essential for life. Management of oxygen metabolism is a fine balance between necessary life support and the highly toxic effects of oxygen and its metabolites. In 1969 it was recognized that superoxide dismutase, a free radical scavenger, formed a part of the routine defense against endogenously generated reactive oxygen species (ROS) [1]. The significance of this observation became apparent 12 years later when superoxide radicals, produced by neutrophils, were identified as the responsible agents for the increased capillary permeability in the ischemic bowel [2]. In short order neutrophils superoxide anion and ROS moved to the forefront of biomedical sciences, where they were perceived predominately as molecular outlaws, posing as a major threat to health [3].Various therapies have been proposed to treat ROSmediated pathology from the use of antagonists of selectins and integrins to prevent neutrophilic infiltration into tissue [4], antioxidant vitamin therapy [5], macrolide antibiotics to inhibit the production of proinflammatory cytokines [6], reduction-oxidation (redox)-sensitive transcription factors [7,8], probiotics [9], peroxisome proliferator-activated receptor agonists and statins [10]. These therapies attempt to block either the activation of the cells responsible for generating excess ROS or the proximal mediators of the ROS-dependent inflammatory response.Another therapeutic strategy to manage ROS production is to modulate the endocrine factors signaling their generation, as occurs with angiotensin II type 1 (AT 1 ) receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors [11,12]. However, little attention has been paid to using the body's natural defenses, offered by endoc...

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Decreased chemotaxis of neutrophils in acromegaly and hyperprolactinemia

Cited by 18 publications

References 23 publications

Prolactin, growth hormone and the immune system in humans

Prolactin, growth hormone and the immune system in humans

Prolactin (PRL) and Its Receptor: Actions, Signal Transduction Pathways and Phenotypes Observed in PRL Receptor Knockout Mice

Modulation of Neutrophil Function by Hormones

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