Burn injury reveals altered phenotype in mannan-binding lectin-deficient mice.
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.
Møller-Kristensen
Mette
M
Laboratory of Developmental Immunology, Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
Hamblin
Michael R
MR
Thiel
Steffen
S
Jensenius
Jens Chr
JC
Takahashi
Kazue
K
D000818:Animals; D002056:Burns / Q000276:immunology* / Q000473:pathology; D003165:Complement System Proteins / Q000276:immunology; D003872:Dermatitis / Q000276:immunology / Q000473:pathology; D020405:Dermis / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D004817:Epidermis / Q000276:immunology* / Q000473:pathology; D006706:Homeostasis / Q000276:immunology; D037601:Mannose-Binding Lectin / Q000235:genetics* / Q000276:immunology*; D020782:Matrix Metalloproteinases / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D010641:Phenotype
D037601:Mannose-Binding Lectin; D003165:Complement System Proteins; D020782:Matrix Metalloproteinases