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pubmed-article:12693661pubmed:abstractTextIslet transplantation is now established as an optional treatment for type I diabetes. However, rates of insulin independence in islet transplant recipients are still low. Although the major source of allograft is derived from brain-dead patient, the nonphysiologic state of brain death (BD) deteriorates organs such as liver and kidney. To determine the effects of BD on islets, a rodent model of BD has been used. Histologically, islets of BD rats showed decreased permeability and impaired integrity of the cell membranes. Flow cytometric analysis showed that CD11b/c-positive cells within islets were slightly increased in BD. This result suggests that BD induces macrophage infiltration into the islets. Moreover, RT-PCR revealed significant augmentation of macrophages-associated inflammatory molecules (IL-1beta, IL-6, TNF-alpha, and MCP-1) in islets from a BD donor. Inducible nitric oxide synthase (iNOS) was weakly expressed, although not reaching statistical significance compared with control. Our results indicate that islets from a BD donor are immunologically activated and have a potential risk factor for early graft loss and a poor long-term function of grafts in clinical setting of islet transplantation. Immunomodulation, to eliminate intraislet immunocytes and/or activated macro phage-associated molecules, might be necessary for the better outcome after islet graft from BD donors.lld:pubmed
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pubmed-article:12693661pubmed:authorpubmed-author:KurodaYoshika...lld:pubmed
pubmed-article:12693661pubmed:authorpubmed-author:SuzukiYasuyuk...lld:pubmed
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pubmed-article:12693661pubmed:articleTitleActivation of macrophage-associated molecules after brain death in islets.lld:pubmed
pubmed-article:12693661pubmed:affiliationDepartment of Gastroenterological Surgery, Graduate School of Medical Sciences, Kobe University, Kobe, Japan.lld:pubmed
pubmed-article:12693661pubmed:publicationTypeJournal Articlelld:pubmed
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