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. Author manuscript; available in PMC: 2008 May 15.
Published in final edited form as: Am J Physiol Renal Physiol. 2008 Feb 27;294(5):F1050–F1058. doi: 10.1152/ajprenal.00461.2007

Figure 5. TLR9 deficiency improves survival, acute kidney injury, splenic apoptosis, and circulating cytokines after polymicrobial sepsis.

Figure 5

(A) Survival curves after CLP for wild-type (dashed line, N = 19) and TLR9-deficient (solid line, N = 16) mice. #, P < 0.05 vs wild-type. Mice were subjected to sham surgery (white bars) or CLP in wild-type (black bars) or TLR9-deficient (gray bars) mice. (B) Number of active caspase3 positive cells in the spleen 24 hr after sham surgery (wild-type, N = 4; TLR9-deficient, N = 4) or CLP (wild-type, N = 7; TLR9-deficient, N = 5). (C) Kidney function 24 hr after sham surgery (wild-type, N = 4; TLR9-deficient, N = 4) or CLP in wild-type (N = 10) and TLR9-deficient (N = 11) mice. (D) Kidney histology scores at 24 hr after surgery (see Methods) for tubules in the renal cortex and outer stripe of the outer medulla (OSOM) at 24 hr after surgery (N = 4-6 per group). (E) Serum TNF-alpha and IL-10 at 24 hr after CLP (N = 6-11 per group). Values are mean ± SE. *, P < 0.05 vs. wild-type.