Fig 2: BAFF positively controls CS-induced inflammation. WT and BAFF deficient mice (BAFF-/-) were exposed to air or CS and sacrificed 16 h after the last exposure. WT mice were instillated with NaCl as control, or with rBAFF (1 µg/mouse) at days 2 and 4 between the second and the third exposure (H). Total cells (A,I) and neutrophils (B,J) in BAL. MPO (C,K), self-dsDNA (D), CXCL5 (E), CXCL1 (G), MMP-9 (F,L), and TIMP-1 (M) levels measured in BALF or lung as indicated. n = 3–7 mice per group. Bar graphs are expressed as mean ± SEM. ns, non-significant; *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.

Fig 3: In vitro CSE stimulation induces BAFF expression in neutrophils and epithelial cells. Bone marrow derived neutrophils (BMDN) were stimulated with medium or medium containing 10% Cigarette Smoke Extrat (CSE) for 4 h. BAFF levels in supernatant (A) and MTT cell viability assay on cellular fraction (B). Murine tracheal epithelial cells (MTEC) were stimulated with medium or medium containing 10% CSE. BAFF was measured in the cellular fraction (C). Stimulation has been performed in triplicate for each condition. Bar graphs are expressed as mean ± SEM. ns, non-significant; *p < 0.05. Mann-Whitney T-test was performed.

Fig 4: Acute CS-exposure induces BAFF expression in airways-recruited neutrophils. Mice were exposed to air (Air) or cigarette smoke (CS) three times a day for 4 days and sacrificed 16 h after the last exposure. Total cells (A), neutrophils (B), and macrophages (C) counted in BAL. MPO levels in BALF (D). BAFF levels, respectively, in BALF and lung (E,F). Tnfsf13 mRNA levels (coding for APRIL) in lung homogenates (G). BAFF immunostaining on BAL cells collected after air or CS exposure: BAFF shown in green and nucleus in blue (DAPI) (H). Fluorescent intensity quantification (I). n = 4–5 mice per group. Bar graphs are expressed as mean ± SEM. ns, non-significant; *p < 0.05 and **p < 0.01.