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9,11-15 Furthermore, activation of FRA-1 has been observed during lung injury induced in guinea pigs by a mustard gas analog (2-chloroethyl ethyl sulfide).
For laser confocal microscopy, 2 lung tissue sections were prepared for each subject, one to stain for activated (phosphorylated) p65 (p-p65) (NF-[kappa]B) and epithelial cell marker (surfactant protein B [SP-B]), and the other to stain for FRA-1 and SP-B.
The degree of interaction between p-p65 and FRA-1 is presented as a correlation coefficient, which reflects the overlap between stains used to label these proteins and takes into account both the intensity and location of signals generated by each stain.
Numbers of lung epithelial cells (SP-B positive) that expressed either p-p65 or FRA-1 were counted, and differences between groups were evaluated by a t test.
The purpose of this study was to determine whether active forms of NF-[kappa]B and FRA-1 are present in lung tissue from patients with ARDS, and whether they are associated with epithelial cells.
Expression of FRA-1 was also studied, because FRA-1 belongs to the activator protein 1 family of transcription factors and members of this family are known to interact with NF-[kappa]B.
No detectable staining for FRA-1 or SP-B was observed in images of negative controls (tissue sections incubated with the secondary antibodies only; Figures 4, C, and 5, C), whereas active FRA-1 was present in lipopolysaccharide-treated A549 cells (positive control in Figure 5, D).
We also counted numbers of lung epithelial cells (SP-B positive) that express either p-p65 or FRA-1 (Figure 6).
Finally, we have observed a partial colocalization between p-p65 and FRA-1 (Figure 7) in lung tissue from ARDS patients.
Both NF-[kappa]B and FRA-1 are involved in transcriptional regulation of various proinflammatory mediators, many of which have been implicated in the development and progression of ALI/ARDS.
It should be noted that in other organ systems blockade of NF-[kappa]B or FRA-1 signaling can promote adverse pathologic responses.