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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: Anesthesiology. 2012 Oct;117(4):822–835. doi: 10.1097/ALN.0b013e31826a4ae3

Figure 2. TLR4 presence and signaling capability is required for full pathologic response to ventilated lung I/R injury.

Figure 2

(A) Inflammatory cytokines and chemokine induction (mRNA) at 1 h post reperfusion measured in lung samples from C3H TLR4mut versus wild type mice using Q-PCR. All measurements were normalized to GAPDH message levels. Each point represents RNA from left lung lower segments of individual WT or C3H TLR4mut mice that underwent I/R surgery. Mice that died before completion of surgery or collection of lungs, or had inadvertent esophageal intubation and required multiple reintubation attempts were excluded from analysis (2 WT and 1 C3H TLR4mut mouse).

(B) H&E histopathology of C3H TLR4 mutant mice and C3H wild type mice left lungs at 3 h post reperfusion after I/R surgery. Each image is representative of histology images from 3 independent surgeries.

(C) Analysis of relative mRNA levels of inflammatory markers (as noted) for left lower lung segments from C57BL/6 wild type mice versus C57BL/6 TLR2 −/− mice at 1 h post reperfusion after I/R surgery. Each point represents RNA from left lung lower segments of individual WT or TLR2ko mice that underwent I/R surgery. One wild type mouse died before completion of surgery and was excluded from analysis.

(D) Histological analysis of C57/BL6 wild type versus TLR2 −/− left lungs following 30 minutes of ischemia and 3 h of reperfusion. Each image is representative of histology images from 2 independent surgeries.

TLR: toll-like receptor; mRNA: messenger RNA; Q-PCR: real-time quantitative polymerase chain reaction; GAPDH: Glyceraldehyde 3-phosphate dehydrogenase;

H&E: hematoxylin and eosin; I/R: ischemia-reperfusion; IL: interleukin; ICAM: intercellular adhesion molecule; CXCL: Chemokine (C-X-C motif) ligand; WT: wild type.