Polarized in vivo expression of IL-11 and IL-17 between acute and chronic skin lesions.
BACKGROUND
In atopic dermatitis (AD) there is evidence of tissue fibrosis involving a number of structural changes, including papillary dermal fibrosis and epidermal hyperplasia. These changes are suggested to be the result of chronic inflammation of the skin. Several remodeling-associated cytokines, including transforming growth factor (TGF) beta1, IL-11, and IL-17, have been shown to be increased in allergic diseases, including asthma.


OBJECTIVE
We investigated TGF-beta1, IL-11, and IL-17 expression in skin biopsy specimens recovered from acute and chronic skin lesions from patients with AD, as well as from uninvolved skin of patients with AD and skin from healthy volunteers. We also examined the correlation between the expression of these cytokines and the extent of total, type I, and type III collagen deposition.


METHODS
We evaluated the expression of TGF-beta1, IL-11, and IL-17 by means of immunohistochemistry. Collagen deposition was assessed by means of immunohistochemistry and van Gieson staining.


RESULTS
TGF-beta1 expression was markedly enhanced in both acute and particularly chronic lesions (P <.001). Although IL-11 expression was significantly increased only in chronic lesions (P <.0001), IL-17 was preferentially associated with acute lesions (P <.005). Although collagen type III deposition was not significantly different among the groups, type I collagen deposition was significantly increased in chronic AD lesions (P <.0005). There was a significant correlation between IL-11 and type I collagen deposition, as well as the number of eosinophils in skin specimens from patients with AD (r (2) = 0.527, and r (2) = 0.622, respectively; P <.0001).


CONCLUSIONS
These results suggest that TGF-beta1, IL-11, and IL-17 are involved in the remodeling of skin lesions in patients with AD. However, IL-11 and IL-17 are preferentially expressed at different stages of the disease. Type I collagen appeared to be the major subtype involved in this repair process.
Toda
Masao
M
Meakins-Christie Laboratories, McGill University, Montreal, Canada.
Leung
Donald Y M
DY
Molet
Sophie
S
Boguniewicz
Mark
M
Taha
Rame
R
Christodoulopoulos
Pota
P
Fukuda
Takeshi
T
Elias
Jack A
JA
Hamid
Qutayba A
QA
D000208:Acute Disease; D000328:Adult; D002908:Chronic Disease; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D016130:Immunophenotyping; D017370:Interleukin-11 / Q000032:analysis*; D020381:Interleukin-17 / Q000032:analysis*; D008875:Middle Aged; D012867:Skin / Q000378:metabolism / Q000473:pathology*; D016212:Transforming Growth Factor beta / Q000032:analysis; D053773:Transforming Growth Factor beta1
D024042:Collagen Type I; D024061:Collagen Type III; D017370:Interleukin-11; D020381:Interleukin-17; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1