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    Diabetes mellitus leads to accumulation of dendritic cells and nerve fiber damage of the subbasal nerve plexus in the cornea (2014)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Leppin, Katja
    Behrendt, Ann-Kathrin
    Reichard, Maria
    Stachs, Oliver
    Guthoff, Rudolf F
    Baltrusch, Simone
    Eule, Johanna C (WE 20)
    Vollmar, Brigitte
    Quelle
    Investigative ophthalmology & visual science
    Bandzählung: 55
    Heftzählung: 6
    Seiten: 3603 – 3615
    ISSN: 0146-0404
    Sprache
    Englisch
    Verweise
    DOI: 10.1167/iovs.14-14307
    Pubmed: 24781935
    Kontakt
    Klein- und Heimtierklinik

    Oertzenweg 19 b
    14163 Berlin
    +49 30 838 62422
    kleintierklinik@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    To evaluate whether nerve fibers of the subbasal nerve plexus (SNP) and dendritic cells (DCs) are in association with each other leading to neuropathy in the diabetic cornea.

    BALB/c mice were injected with streptozotocin (STZ) for 5 days for induction of diabetes mellitus (DM) or with vehicle solution (control). B6.VLep(ob/ob) (ob/ob) mice served as an obese and glucose-intolerant DM type 2 (DM II) model and lean B6.VLep(ob/+) (ob/+) mice as respective controls. Using in vivo corneal confocal microscopy (CCM), nerve fibers and DCs were quantified over a period of 9 weeks and additionally analyzed by in vitro immunofluorescence whole-mount staining.

    In STZ-diabetic mice, CCM revealed an increase of DC density (DCD) in contrast to controls, whereas nerve fiber density (NFD) was decreased with duration of DM. In ob/ob mice, DCD was 3-fold higher than in both ob/+ mice and STZ-diabetic mice. Whole-mount staining displayed CD11c(+) and major histocompatibility complex (MHC) class II(+) mature DCs in colocalization with class III β-tubulin(+) nerve fibers in the cornea.

    Hyperglycemia leads to corneal DC infiltration, and obesity aggravates this immune response. The direct contact between DCs and the SNP can be assumed to be a trigger of nerve fiber damage and thus a contributing factor to polyneuropathy in diabetic corneas.