Tissue damage due to CXCL8-mediated neutrophil influx.
Representative lung sections of mice treated with (A) 50 µl phosphate buffer saline (PBS), (B) 10 µg CXCL8 dimer in 50 µl PBS after 6 h, and (C) 107 PFU of human metapneumovirus in 50 µl PBS after 24 h. Lungs were fixed with 10% formaldehyde in PBS, and histological sections were stained with haematoxylin and eosin (20× magnification; scale bar = 200 µm). Markers of tissue damage such as airway obliteration (arrow heads), peribronchiolar (short arrow), and perivascular (long arrow) inflammatory cell accumulation are obvious in the virus-infected lung tissue, and are completely absent in CXCL8 dimer treated lung tissue. (D) Total protein in cell free BALF from mice treated with 10 µg of CXCL8 WT, trapped monomer at various time intervals. Statistical analyses show no significant differences in protein levels among different CXCL8 variants at all time points.
