Epidermal Growth Factor Relieves Inflammatory Signals in Staphylococcus aureus-Treated Human Epidermal Keratinocytes and Atopic Dermatitis-Like Skin Lesions in Nc/Nga Mice

Figure 2

Recombinant human epidermal growth factor (rhEGF) downregulated the expression of TLR-2 and related signaling markers induced by heat-killed S. aureus (HKSA). (a) 10 ng/mL of rhEGF did not induce TLR-2 mRNA expression. However, HKSA with a multiplicity of infection (MOI) of 10 (10 MOI HKSA) increased TLR-2 mRNA expression, which was inhibited by rhEGF 10 ng/mL. (b) Similarly, 10 ng/mL of rhEGF did not affect TLR-2 protein expression. 10 MOI HKSA induced TLR-2 protein expression, which was downregulated by 10 ng/mL of rhEGF. (c) 10 ng/mL of rhEGF did not affect p38 MAPK mRNA expression. However, 10 MOI HKSA increased the expression of p38α and p38δ; such expression was inhibited by 10 ng/mL of rhEGF. In contrast, 10 MOI HKSA reduced the expression of p38β and p38γ; such expression was induced by 10 ng/mL of rhEGF. (d) 10 MOI HKSA induced mRNA expression of the TLR-2-related cell signaling markers NFκB and ERK (MAPK1 and MAPK3). Cell signaling mRNA expression was downregulated by 10 ng/mL of rhEGF. The results are presented as the mean ± STDEV, representative of three separate experiments. Asterisks indicate statistically significant differences ( < 0.05, < 0.01).

(a)

(b)

(c)

(d)