Sjögren’s Syndrome Antigen B Acts as an Endogenous Danger Molecule to Induce Interleukin-8 Gene Expression in Polymorphonuclear Neutrophils
Fig 5
Signaling pathways for rSSB-induced IL-8 production in normal human PMNs and HL-60 (RA) cells.
A, Activation and phosphorylation of p38, ERK1/2 and JNK MAPK pathways by rSSB (10 μg/ml) in normal human PMNs. B, Activation and phosphorylation of p38 and ERK1/2 MAPK pathways by rSSB (10 μg/ml) in HL-60 (RA) cells. A representative blot of 3 independent experiments is shown in (A) and (B). C, The effects of specific inhibitors for p38 (SB203580, SB 10 μM), MEK-1 (PD98059, PD, 10 μM), p38 and MEK-1 (SB + PD, 10 μM each), and Gαi-protein-coupled receptors (pertussis toxin, PTX, 100 ng/ml) on rSSB (10 μg/ml)- or LPS (100 ng/ml) induced IL-8 production were compared. The relative ratio of IL-8 production in the medium pretreatment group was set at 1, and multiple comparisons were adjusted by Bonferroni correction. D, Nuclear translocation of NF-κB subunits p65 and p50 induced by rSSB (10 μg/ml) at 1 hour compared to medium control in HL-60 (RA) cells. *p<0.05. E, Nuclear translocation of NF-κB subunits p65 and p50 induced by rSSB (10 μg/ml) at 1 hour compared to medium control in normal human PMNs. A representative result of 2 independent experiments is shown in E.