(A) The major canonical pathways significantly affected by KP35 are shown in order of statistical significance. Spectral counts for the 1,638 proteins in the pooled bronchoalveolar lavage fluid (n = 3) were uploaded into ingenuity pathway analysis software. Numbers above the columns are the number of proteins within each group, with colored bars representing the proportion of up- and downregulated genes with KP35 infection as compared with PBS control. Subgroup analysis reflects the differential abundance of specific proteins in KPPR1 and KP35 infection, normalized to PBS controls. This analysis identified (B) actin cytoskeletal remodeling, (C) phagocytosis, and (D) Ca²⁺/calpain signaling pathways as differentially affected by KP35 as compared with KPPR1. (E) Functional confirmation of the importance of Ca²⁺ fluxes in phagocytic killing. Percentage of KPPR1 (blue) and KP35 (red) (MOI of 1) killing by neutrophils in the presence of calpeptin (CPEP) compared with DMSO control. *P < 0.05, Mann-Whitney test, n = 8. (F) Differential activation of Ca²⁺ fluxes by KP35 and KPPR1. Ca²⁺ fluxes were measured in murine neutrophils (NEUTs) loaded with AM/Fluo-4 prior to stimulation with KP35 and KPPR1 (MOI of 100) or media alone followed by thapsigargin (1 μM) as a positive control. Total field fluorescence was measured at each time point using ImageJ. **P < 0.05, 2-way ANOVA, Bonferroni’s correction for multiple comparisons. Data were compiled from E or are representative (F) of at least 3 independent experiments.