AI Article Synopsis

  • The study investigates the role of cytokines, specifically interleukin-8 (IL-8), in the development of growth hormone (GH)-producing pituitary adenomas, which can lead to serious health issues.
  • Researchers obtained human pituitary tumor tissue from patients with acromegaly, cultured the cells, and examined their responses to various stimuli (GHRH and somatostatin).
  • The findings showed that cultured adenoma cells released IL-6 and IL-8 in response to interleukin-1β, suggesting these cytokines may play a significant role in tumor growth and could lead to targeted therapies.

Article Abstract

Objective: Pituitary adenomas cause morbidity and mortality due to their localization and influence on pituitary hormone secretion. Although the pathogenesis of pituitary adenomas is unclear, studies have indicated that cytokines are involved. We investigated the role of cytokines, in particular interleukin (IL)-8, in the pathogenesis of growth hormone (GH) producing tumours.

Design: Human somatotroph adenoma tissue was obtained from patients undergoing surgery for acromegaly. The tissue underwent mechanical and enzymatic digestion, was washed, suspended and cultured in 24-chamber plates. After stimulation/inhibition supernatants were harvested. As control of growth hormone producing properties of the cultured cells, GH releasing hormone (GHRH) stimulated and somatostatin inhibited the GH response.

Results: The cultured adenoma cells released both IL-6 and IL-8 and the secretion was inhibited by GHRH and somatostatin. IL-1β dose-dependently stimulated GH, IL-6 and IL-8 secretion.

Conclusion: Using cultured primary somatotroph adenoma cells as a dynamic method, we found a consistent release not only of IL-6 as described previously, but also of IL-8. This finding could be important for reassessing a role of these cytokines in the pathogenesis of pituitary tumour growth and function, and thus form a basis for targeted therapy. In line with previous studies, our results further indicated a common physiological or pathophysiological reaction of endocrine cells to cytokine stimulation.

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Source
http://dx.doi.org/10.1016/j.ghir.2011.03.005DOI Listing

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