QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, January 31, 2007, 27(5):1161-1166; doi:10.1523/JNEUROSCI.4560-06.2007

This Article Full Text Full Text (PDF) Submit an eLetter View eLetters for this paper Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Johnson, D. R. Articles by Freund, G. G. Search for Related Content PubMed PubMed Citation Articles by Johnson, D. R. Articles by Freund, G. G.

 Previous Article  |  Next Article 

Brief Communications
Acute Hypoxia Activates the Neuroimmune System, Which Diabetes Exacerbates

Daniel R. Johnson,¹ Jason C. O'Connor,² Matthew E. Hartman,¹ Richard I. Tapping,³ and Gregory G. Freund^1,2,4

¹Department of Animal Sciences, ²Division of Nutritional Science, ³Department of Medical Microbiology, and ⁴Department of Pathology, Integrative Immunology and Behavior Program, University of Illinois, Urbana, Illinois 61801

Correspondence should be addressed to Dr. Gregory G. Freund, Department of Pathology, College of Medicine, 506 South Mathews Avenue, University of Illinois at Urbana Champaign, Urbana, IL 61801. Email: freun{at}uiuc.edu

Acute hypoxia is experienced in an array of ailments and conditions, including asthma, chronic obstructive pulmonary disease, heart failure, sleep apnea, acute hypotension, and blast lung injury. Classically, infection activates the neuroimmune system, causing loss of interest in the social environment. We report that the non-infectious stimulus acute hypoxia triggers neuroimmune system activation (NSA), causing loss of interest in the social environment, and that recovery from hypoxia-induced NSA is impaired in a mouse model of type 2 diabetes. Importantly, recovery from the behavioral consequences of hypoxia-induced NSA was nearly ablated in MyD88 (myeloid differentiation factor 88) knock-out mice and in mice intracerebroventricularly administered the caspase-1 inhibitor ac-YVAD-CMK (ac-Tyr-Val-Asp-2,6-dimethylbenzoyloxymethylketone). Diabetic mice had prolonged recovery from NSA that could be halved by administration of subcutaneous interleukin-1 (IL-1) receptor antagonist (RA). These results show that acute hypoxia activates the IL-1ß arm of the neuroimmune system, which diabetes exacerbates and treatment with IL-1RA ameliorates.

Key words: IL-1ß; IL-1 receptor antagonist; innate immunity; hypoxia; neuroimmunity; type 2 diabetes; caspase-1; myeloid differentiation factor 88

---

Received Oct. 20, 2006; revised Dec. 19, 2006; accepted Dec. 24, 2006.

Correspondence should be addressed to Dr. Gregory G. Freund, Department of Pathology, College of Medicine, 506 South Mathews Avenue, University of Illinois at Urbana Champaign, Urbana, IL 61801. Email: freun{at}uiuc.edu

This article has been cited by other articles:

				C. L. Sherry, S. S. Kim, and G. G. Freund Accelerated Recovery from Acute Hypoxia in Obese Mice Is Due to Obesity-Associated Up-Regulation of Interleukin-1 Receptor Antagonist Endocrinology, June 1, 2009; 150(6): 2660 - 2667. [Abstract] [Full Text] [PDF]

				D. R. Johnson, C. L. Sherry, J. M. York, and G. G. Freund Acute Hypoxia, Diabetes, and Neuroimmune Dysregulation: Converging Mechanisms in the Brain Neuroscientist, June 1, 2008; 14(3): 235 - 239. [Abstract] [PDF]

eLetters:

Read all eLetters

Metabolic mediator in diabetic acidosis

Heikki Savolainen

J. Neurosci. Online, 1 Feb 2007 [Full text]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help