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. 2013 Nov 1;306(1):L69–L79. doi: 10.1152/ajplung.00205.2013

Fig. 7.

Fig. 7.

iNKT cell-produced IL-17 and alveolar macrophage-produced TNF-α mediate CXCL1 production by ATII cells via NADPH oxidase. An in vitro model of HR was used to evaluate the effect of primary iNKT cells and alveolar macrophages on ATII cells. A: after HR, iNKT cells produce IL-17, macrophages (Mac) produce TNF-α, and ATII cells produce CXCL1 vs. normoxic (Norm) controls. *P < 0.05 vs. Norm; n = 6–8/group. B: CXCL1 production was significantly enhanced upon conditioned media transfer (CMT) from HR-exposed macrophages (MacHR) to HR-exposed ATII cells (ATIIHR) compared with ATIIHR alone. No change in CXCL1 production was observed by CMT from HR-exposed iNKT cells (iNKTHR) to HR-exposed ATII cells (ATIIHR) compared with ATIIHR alone. However, a synergistic increase in CXCL1 production was observed upon combined CMT from iNKTHR and MacHR to ATIIHR, which was significantly blocked by apocynin (Apo) pretreatment of ATIIHR cells. *P < 0.05 vs. ATIINorm; **P < 0.05 vs. ATIIHR; #P < 0.05 vs. MacHR (CMT) ATIIHR; ##P < 0.05 vs. iNKTHR/MacHR (CMT) ATIIHR; n = 8/group.