Document Detail


Nerve-Langerhans cell interactions in diabetes and aging.
MedLine Citation:
PMID:  23059889     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cutaneous infections are a leading cause of hospitalization of diabetic patients. Langerhans cells (LCs) are antigen-presenting cutaneous dendritic cells that protect against infections, and effects of diabetes and aging on these cells are unclear. We examined LCs in footpads of rats with streptozotocin-induced diabetes at 3 months of age following 4 weeks of diabetes, and at 6 months following 16 weeks of diabetes. Immunostaining of LCs using the selective marker protein langerin showed cutaneous LC composition increased between 3 and 6 months of age owing to increased LC numbers and size in control rats. In diabetic rats, LC numbers increased with age but, unlike 6 month old controls, cell size did not, suggesting that diabetes impairs the increase in cell size that is a hallmark of LC maturation. Diabetes reduced LC numbers after 4 weeks and numbers and sizes following 16 weeks. We examined the relation between LC and innervation and found that, while axon density decreased with aging, it was not affected by 16 weeks of diabetes. However, LCs expressing the neuronal marker PGP9.5 represented a source of error in axonal counts. These findings support the hypothesis that diabetes substantially impacts LC proliferation and maturation independent of effects on cutaneous innervation. Accordingly, the interactions of diabetes and aging on LCs may be important factors in predisposing diabetic patients to cutaneous ulcers and infections.
Authors:
A L N Doss; P G Smith
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Histology and histopathology     Volume:  27     ISSN:  1699-5848     ISO Abbreviation:  Histol. Histopathol.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-10-12     Completed Date:  2013-03-21     Revised Date:  2013-07-22    
Medline Journal Info:
Nlm Unique ID:  8609357     Medline TA:  Histol Histopathol     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  1589-98     Citation Subset:  IM    
Affiliation:
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging / metabolism,  pathology*
Animals
Antigens, Surface / metabolism
Cell Differentiation
Cell Proliferation
Diabetes Complications / etiology,  metabolism,  pathology
Diabetes Mellitus / metabolism,  pathology
Diabetes Mellitus, Experimental / metabolism,  pathology*
Female
Humans
Immunohistochemistry
Langerhans Cells / metabolism,  pathology*
Nerve Fibers / metabolism,  pathology
Neurons / metabolism,  pathology*
Rats
Rats, Sprague-Dawley
Skin / innervation,  metabolism,  pathology
Skin Ulcer / etiology,  metabolism,  pathology
Ubiquitin Thiolesterase / metabolism
Grant Support
ID/Acronym/Agency:
1F31 DK083845/DK/NIDDK NIH HHS; 1R01 NS053796/NS/NINDS NIH HHS; P30 HD002528/HD/NICHD NIH HHS; P30 HD002528/HD/NICHD NIH HHS; R01 NS053796/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Surface; EC 3.1.2.-/PGP9.5 protein, rat; EC 3.1.2.15/Ubiquitin Thiolesterase
Comments/Corrections

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