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Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice.

Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Research Abstract Details 

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  • Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Abstract Text:

    robert gyurkoRobert Gyurko,camille c siqueiraCamille C Siqueira,nathaniel caldonNathaniel Caldon,li gaoLi Gao,alpdogan kantarciAlpdogan Kantarci,thomas e van dykeThomas E Van Dyke,

    The role of polymorphonuclear neutrophils (PMN) in mediating diabetic tissue damage to the periodontium was investigated in a novel model of chronic hyperglycemia, the Akita mouse. Induction of acute peritoneal inflammation in wild-type (WT) and Akita mice resulted in exaggerated IL-6 response in Akita mice (2.9-fold increase over WT values) and a markedly increased chemokine response (KC, 2.6-fold; MCP-1, 2.6-fold; and MIP-1alpha, 4.4-fold increase over WT values). Chemotaxis to both fMLP and WKYMVm was significantly reduced in isolated Akita PMN compared with WT PMN as measured in a Boyden chamber. Superoxide release in contrast was significantly increased in Akita PMN as measured with cytochrome c reduction. Bone marrow-derived Akita PMN showed partial translocation of p47phox to the cell membrane without external stimulation, suggesting premature assembly of the superoxide-producing NADPH oxidase in hyperglycemia. In vivo studies revealed that ligature-induced periodontal bone loss is significantly greater in Akita mice compared with WT. Moreover, intravital microscopy of gingival vessels showed that leukocyte rolling and attachment to the vascular endothelium is enhanced in periodontal vessels of Akita mice. These results indicate that chronic hyperglycemia predisposes to exaggerated inflammatory response and primes leukocytes for marginalization and superoxide production but not for transmigration. Thus, leukocyte defects in hyperglycemia may contribute to periodontal tissue damage by impairing the innate immune response to periodontal pathogens as well as by increasing free radical load in the gingival microvasculature.

    Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Publishing Authors By Initials

    r gyurkoR Gyurko,cc siqueiraCC Siqueira,n caldonN Caldon,l gaoL Gao,a kantarciA Kantarci,te van dykeTE Van Dyke,

    For similar beta-glucans: zymosan research abstracts see: beta-glucans: zymosan research

    PUBMED ID PMID:

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    Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    VOLUME: 177

    Page Numbers: 7250-6

    Journal Abbreviation: J. Immunol.

    ISSN: 0022-1767

    DAY: 15

    MONTH: Nov

    YEAR: 2006

    Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Keywords Mesh Terms:

    KEYWORDS: Zymosan

    MESH TERMS: toxicity

    Chemical & Substance for Abstract: Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice. Information

    Substance Name: Zymosan

    Registry Number: 9010-72-4

    Grant and Affiliation Information for Chronic hyperglycemia predisposes to exaggerated inflammatory response and leukocyte dysfunction in Akita mice.

    AFFILIATION: Department of Periodontology and Oral Biology, Boston University, Boston, MA 02118, USA. gyurko@bu.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDCR

    GRANT: DE16933

    ACRONYM: DE

    MEDLINETA: J Immunol

    REFSOURCE:

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    ACCESSION NUMBER:

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