Influenza Virus Infects Epithelial Stem/Progenitor Cells of the Distal Lung: Impact on Fgfr2b-Driven Epithelial Repair (original) (raw)
Fig 2
EpiSPC are resistant to apoptosis and show a high proliferative response after PR/8 infection which is mediated by Fgf10/Fgfr2b signaling.
(A) Proliferation rates of the given epithelial cell subsets was analysed in PR/8 infected wt mice by FACS quantification of Ki67+ cells at the indicated time points pi. (B) Apoptosis of each EpCam+ subset was quantified by FACS (Annexin V+ proportions) at d7 post PR/8 infection and of non-infected wt mice. (C) Expression of Fgfr2b on EpiSPC at the given time points post PR/8 or mock infection was quantified by FACS and is given as MFI (median fluorescence intensity) of Fgfr2b ab minus MFI of matched isotype control. The proliferative response of the EpCam+ cell subsets was quantified by FACS at d7 pi in Rosa26 rtTA/+ ;tet(O)sFgfr2b/+ (D) Rosa26 rtTA/+ ;tet(O)Fgf10/+ mice (E) and Fgf7 -/- mice (F) compared to non-dox-induced or wt littermates. Bar graphs represent means ± SD of n = 4–6 independent experiments; * p<0.05; **p<0.01; +dox, doxycycline food; -dox, normal diet.