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. 2014 May;82(5):1994–2005. doi: 10.1128/IAI.01578-14

FIG 5.

FIG 5

TLR stimulation reversed antibiotic treatment-induced reduction of nondefensin proteins and NF-κB DNA binding activity of the intestinal mucosa. (A) TLR stimulation with dead E. coli oral supplementation significantly induced Reg3β, Reg3γ, CRP-ductin, and RELMβ mRNA levels in the intestinal mucosa of antibiotic-treated mice. Dead S. aureus oral supplementation significantly increased the expression of CRP-ductin in the intestinal mucosa. (B) Immunoblotting assays showed that TLR stimulation with dead E. coli induced a significant increase in RegIIIβ, RELMβ, and TLR4 protein expression in antibiotic-treated mice. Dead S. aureus supplementation induced a significant increase in TLR4 protein expression in antibiotic-treated mice. TLR stimulation with dead E. coli or S. aureus had no effect on the expression of α-defensin 4. (C) Antibiotic treatment for 6 days (IMAb-6) significantly decreased NF-κB DNA binding activity in the intestinal mucosa. Dead E. coli or S. aureus supplementation for 2 days reversed the inhibitory effect of antibiotics on NF-κB DNA binding activity in the intestinal mucosa. NS, nonspecific band; Cont, control; IMab-4, intramuscular antibiotic treatment for 4 days; IMab-6, intramuscular antibiotic treatment for 6 days; *, P < 0.05; **, P < 0.01; ***, P < 0.001. n = 3 to 5/group.

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