Effects of lipopolysaccharide (LPS) treatment are partially inhibited in Toll-like receptor 4 (TLR4)-deficient mice and blocked in Myeloid differentiation factor 88 (MyD88)-deficient mice. (A-F) Representative of H&E (A-C), CD163 (D-F), and arginase-1 (ARG-1) (G-I) staining cross section of murine skin after LPS-pump in wild-type (WT) (A, D, G), TLR4-/- (B, E, H) or MyD88-/- (C, F, I) mice. (J- R) Gene expression in skin of WT, TLR4-/- and MyD88-/- mice treated for 1 week with PBS: WT (n = 6, open circles) TLR4-/- (n = 2, open triangles), MyD88-/- (n = 4, open diamonds); or with LPS: WT (n = 13, solid circles) TLR4-/- (n = 5, solid triangles), MyD88-/- (n = 6, solid diamonds); *P <0.05, ** P <0.01, *** P <0.001, ns = not significant. Proinflammatory genes: (J) IL-1β, (K) TNF-α, and (L) IL-6. Macrophage markers: (M) CD11b; M2 and M1 macrophages: (N) YM1 and (O) NOS2. Pro-fibrotic genes: (P) thrombospondin 1 (THBS1), (Q) tissue inhibitor metalloproteinase 1 (TIMP1), (R) plasminogen activator inhibitor-1 (PAI-1) and (S) osteopontin 1 (SPP1).