Ra. Taha et al., Evidence for increased expression of eotaxin and monocyte chemotactic protein-4 in atopic dermatitis, J ALLERG CL, 105(5), 2000, pp. 1002-1007
Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease a
ssociated with tissue eosinophilia and the activation of T lymphocytes. The
novel eosinophil chemoattractants, eotaxin and monocyte chemotactic protei
n (MCP)-4, are up-regulated at sites of allergic inflammation, Set their co
ntribution to the pathophysiologic mechanisms of AD remains to be determine
d.
Objective: We sought to investigate the expression of eotaxin and MCP-4 in
acute and chronic lesions from patients with AD and to determine their rela
tionship to the numbers of resident inflammatory cells.
Methods: With use of in situ hybridization, the expression of eotaxin and M
CP-4 messenger RNA (mRNA) in skin biopsy specimens from patients with acute
and chronic AD skin Lesions was compared with that of uninvolved skin from
these patients and skin from healthy volunteers.
Results: There was a constitutive expression of eotaxin and MCP-4 mRNA in s
kin biopsy specimens from healthy subjects. Positive signal for chemokine m
RNA was observed both within the epidermis and inflammatory cells macrophag
es, eosinophils. and T cells of the subepidermis in AD skin lesions. Within
the subepithelium acute and chronic skin lesions exhibited a significant i
ncrease in the numbers of eotaxin and MCP-4 mRNA-positive cells compared wi
th uninvolved skin (P < .01), whereas the numbers of eotaxin and MCP-4 mRNA
-positive cells were significantly higher in chronic AD compared with acute
AD skin lesions (P < .005. P < .001, respectively). Correlations were obse
rved between the expression of eotaxin and MCP-4 mRNA and the presence of e
osinophils and macrophages, respectively, in AD lesions (r(2) = 0.84, r(2)
= 0.94).
Conclusion: There is an increased expression of eotaxin and MCP-4 in acute
and chronic lesions, suggesting that these chemotactic factors play a major
role in the pathophysiologic mechanisms of AD.