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. 2007 Aug 27;75(11):5353–5360. doi: 10.1128/IAI.00922-07

FIG. 2.

FIG. 2.

NU14 and clinical E. coli isolates suppress urothelial CXCL-8 and CXCL-6 secretion. (A) TEU-1 cells were treated with E. coli strain NU14 or HB101/p1-17 in the presence (+) or absence (−) of 1.5 ng/ml TNF-α. Following culture for 4 h, culture supernatants were harvested, and CXCL-8 secretion was measured by ELISA. (B) TEU-1 cells were treated for 4 h with TNF-α, NU14, HB101/p1-17, or clinical isolates 8 to 64 from the ECOR panel (MOI of 250:1), culture supernatants were harvested, and CXCL-8 secretion was measured by ELISA. (C and D) TEU-1 cells were treated for 4 h with E. coli strain NU14, HB101/p1-17, or various clinical isolates (8 to 64) in the presence (+) or absence (−) of 1.5 ng/ml TNF-α, and CXCL-8 (C) or CXCL-6 (D) secretion was measured by ELISA. Error bars reflect the standard deviations of triplicate samples. Asterisks indicate statistically significant differences between (A) TNF-α-treated and NU14-infected and (B) NU14- and ECOR strain 14- and 51-infected TEU-1 cells.