Cited by 238Growth Hormone and Insulin-like Growth FactorsCytokine Signaling Pathways and InteractionsAdipokines, Inflammation, and Metabolic Diseases

Regulation of IGF-I function by proinflammatory cytokines: At the interface of immunology and endocrinology

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O’Connor, Jason C., McCusker, Robert H., Strle, Klemen, Johnson, Rodney W., Dantzer, Robert, Kelley, Keith W.·2008·Cellular Immunology

Abstract

During the past decade, the immune and endocrine systems have been discovered to interact in controlling physiologic processes as diverse as cell growth and differentiation, metabolism, and even human and animal behavior. The interaction between these two major physiological systems is a bi-directional process. While it has been well documented that hormones, including prolactin (PRL), growth hormone (GH), insulin-like growth factor-I (IGF-I), and thyroid-stimulating hormone (TSH), regulate a variety of immune events, a great deal of data have accumulated supporting the notion that cytokines from the innate immune system also affect the neuroendocrine system. Communication between these two systems coordinates processes that are necessary to maintain homeostasis. Proinflammatory cytokines often act as negative regulatory signals that temper the action of hormones and growth factors. This system of 'checks and balances' is an active, ongoing process, even in healthy individuals. Dysregulation of this process has been implicated as a potential pathogenic factor in the development of co-morbid conditions associated with several chronic inflammatory diseases, including type 2 diabetes, cardiovascular disease, cerebrovascular disease, inflammatory bowel disease, rheumatoid arthritis, major depression, and even normal aging. Over the past decade, research in our laboratory has focused on the ability of the major proinflammatory cytokines, tumor necrosis factor (TNF)alpha and interleukin (IL)-1beta, to induce a state of IGF resistance. This review will highlight these and other new findings by explaining how proinflammatory cytokines induce resistance to the major growth factor, insulin-like growth factor-I (IGF-I). We also highlight that IGF-I can induce resistance or reduce sensitivity to brain TNFalpha and discuss how TNFalpha, IL-1beta, and IGF-I interact to regulate several aspects of behavior and cognition.

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Crossref · 10.1016/j.cellimm.2007.09.010

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  1. [96]Moldawer LL, Copeland EM., 3rd Proinflammatory cytokines, nutritional support, and the cachexia syndrome: interactions and therapeutic options. Cancer. 1997;79:1828–1839. [PubMed] [Google Scholar]

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Authors
O’Connor, J. C., McCusker, R. H., Strle, K., Johnson, R. W., Dantzer, R., & Kelley, K. W.
Affiliations
University of Illinois Urbana-Champaign (US)
Corresponding author
Kelley, Keith W.
Venue
Cellular Immunology
Publisher
Elsevier BV
Published
2008
Volume
252
Issue
1-2
Pages
91-110
ISSN
0008-8749 (ISSN-L)
OpenAlex
W2006585084
Cited by
238
References
170
Citations by year
2026: 5 · 2025: 7 · 2024: 6 · 2023: 10 · 2022: 11 · 2021: 13 · 2020: 11 · 2019: 11 · 2018: 13 · 2017: 15 · 2016: 16 · 2015: 12 · 2014: 18 · 2013: 16 · 2012: 15
FWCI
2.72
Type
journal article
Language
en
Open access
Locations
  • Cellular Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (AG029573, AG 16710, R01AG023580, R01AG016710, AG 023580, R01AG029573)
  • National Institute of Mental Health (MH-079829, R01MH079829, MH 71349, R01MH071349, R01MH051569, MH51569)
  • National Institute of Allergy and Infectious Diseases (AI 50422, R01AI050442)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
insulin-like growth factor I, inflammatory cytokines, TNF-α, IL-1β, endocrine-immune interaction, neuroendocrine regulation, growth hormone, prolactin, thyroid-stimulating hormone, chronic inflammation, type 2 diabetes, cognitive function, behavior
MeSH terms
Animals, Brain, Humans, Insulin-Like Growth Factor I, Tumor Necrosis Factor-alpha, Mice, Interleukin-1beta

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