Skip to main content
Fig. 3 | Respiratory Research

Fig. 3

From: Increased susceptibility to organic dust exposure-induced inflammatory lung disease with enhanced rheumatoid arthritis-associated autoantigen expression in HLA-DR4 transgenic mice

Fig. 3

Expression of lung autoantigens, serum inflammatory markers, and autoantibodies following ODE exposure. A Confocal images of lung tissue from treatment groups stained for citrulline (CIT)- and malondialdehyde-acetaldehyde (MAA)-modified proteins as well as vimentin, with nuclei staining by DAPI (blue). Images were analyzed using Zen 2012 software (Zeiss). Bar graphs depict mean integrated density (+ SD) of B CIT- or C MAA-modified proteins, and D vimentin, quantified per each mouse. E R2-values demonstrating co-localization of MAA-CIT, CIT-Vimentin, and MAA-Vimentin within each treatment group. Panels FH demonstrate serum levels of the murine acute phase reactant protein, pentraxin-2 (F), serum levels of IgG antibody to MAA-modified proteins utilizing human serum albumin, collagen type II, and vimentin as the substrate antigen (G), and BALF levels of IgG antibody to MAA (H), all quantified by ELISA. Statistical differences versus saline-treated mice are indicated by #p < 0.05, ##p < 0.01, ###p < 0.001, ####p < 0.0001. Brackets between groups represents significant gene-ODE interaction (P-int) and “a” (p < 0.05) is WT-ODE vs. DR4-ODE. RU: relative units. Line scale is 100 μm

Back to article page