Fig. 2: Ac-PGP drives tissue damage and Lacto LBP reduces neutrophilic inflammation.

Ac-PGP and LPS exposure each in combination with hyperoxia (HO) resulted in severe alveolar hypoplasia and simplification. A Treatment with RTR (arginine-threonine-arginine) improved alveolar structure. H&E staining, 4x magnification. B RAC decreased upon dosing with Ac-PGP or LPS (N = 120 samples) and C MPO expression increased in Ac-PGP exposure in HO (P = 0.0451; Air N = 11, Air+Ac-PGP N = 8, HO N = 8, HO+Ac-PGP N = 5 mice). D Right ventricular hypertrophy (RVH) increased in Ac-PGP + HO mice. (P = 0.028; N = 4 mice). E RAC improved upon treatment with RTR. N = 120 samples. F MPO expression increased upon exposure to LPS + HO and reduced upon RTR treatment (P = 0.0079; Air N = 10, Air + RTR N = 9, HO N = 5, HO + LPS + RTR N = 5 mice). G RVH decreased in LPS + HO mice treated with RTR (P = 0.0187; N = 4 mice). Mann–Whitney U-test, Kruskal–Wallis, Dunn’s multiple comparisons test. H Hyperoxia exacerbated alveolar simplification in mice exposed to E. coli intranasally, while intratracheal LBP treatment improved tissue structure in E. coli + HO mice. H&E staining, 4x magnification. I RAC decreased in HO + E. coli exposure and restored to normal with LBP treatment. Air N = 7, Air + E. coli N = 5, Air + E. coli + Lacto N = 5, HO groups N = 5 mice each. J BAL MMP-9, K NE, L MPO, M IL-6, and N CRP decreased upon treatment with LBP. One-way ANOVA, Tukey’s multiple comparisons test. Air N = 7, Air + E. coli N = 10, Air + E. coli + Lacto N = 5, HO N = 6, HO + E. coli N = 8, HO + E. coli + Lacto N = 5 mice. Bars represent the median ± interquartile range. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.