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Jens Christian Jensenius

Burn injury reveals altered phenotype in mannan-binding lectin-deficient mice

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Burn injury destroys skin, the second largest innate immune organ in the body, and triggers chaotic immune and inflammatory responses. The pattern recognition molecule, mannan-binding lectin (MBL), plays an important role in the first-line host defense against infectious agents. MBL initiates the lectin complement pathway and acts as an opsonin. Recent studies suggest that MBL also modulates inflammatory responses. We report that local responses after burn in MBL null mice differ from those found in wild-type (WT) mice in the following important biological markers: spontaneous eschar separation, thinned epidermis and dermis, upregulation of soluble factors including cytokines, chemokines, cell adhesion molecules, a growth factor-binding protein, and matrix metalloproteinases. Mice lacking C1q, C4, or C3 did not show the lack of eschar separation seen in MBL null-burn phenotype. These findings implicate MBL as an important molecule in the maintenance of the homeostatic balance.
Original languageEnglish
JournalJournal of Investigative Dermatology
Volume127
Issue6
Pages (from-to)1524-31
Number of pages8
ISSN0022-202X
DOIs
Publication statusPublished - 2007

    Research areas

  • Animals, Burns, Complement System Proteins, Dermatitis, Dermis, Disease Models, Animal, Epidermis, Homeostasis, Mannose-Binding Lectin, Matrix Metalloproteinases, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Phenotype

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