Fig. 3: SCFA receptor deficiency does not influence pulmonary cytokine production and immune cell infiltration during K. pneumoniae infection.

A Conventionally colonized (CONV) or antibiotic (ABX)-treated WT and Ffar2/Ffar3^-/- mice were infected with K. pneumoniae for 24 h and bacterial loads (CFU) in lungs were assessed (n = 18 for CONV WT; n = 18 for ABX WT; n = 17 for CONV Ffar2/Ffar3^-/-; n = 17 for ABX Ffar2/Ffar3^-/-). B WT mice treated with antibiotics (ABX) were additionally given SCFA or NaCl. Lung bacterial loads were assessed after 24 h (n = 13 for NaCl; n = 15 for Ace; n = 15 for Pro; n = 15 for But). C WT and Ffar2/Ffar3^-/- mice treated with antibiotics (ABX) were additionally given acetate (200 mM, Ace) or NaCl, and lung bacterial loads were assessed (n = 4 for NaCl WT; n = 6 for Ace WT; n = 4 for NaCl Ffar2/Ffar3^-/-; n = 5 for Ace Ffar2/Ffar3^-/-). D–F Conventionally housed mice were intranasally infected with K. pneumoniae for 12 h, cytokine levels in BALF were measured by multiplex ELISA (n = 12 for WT; n = 13 for Ffar2/Ffar3^-/-) or AMs (alveolar macrophages), PMNs (pulmonary neutrophils), IMs (inflammatory monocytes), CD11b⁺ DCs (dendritic cells), CD103b⁺ DCs, and NK cells (natural killer cells) in lung tissue were analyzed by FACS (n = 19 for WT; n = 18 for Ffar2/Ffar3^-/-). Kruskal-Wallis test followed by Dunn´s multiple comparison was applied to the bacterial load datasets (A–C). Mann-Whitney U test (two-tailed) was applied for lung cell populations and cytokines (D–F). Values are shown as median, each dot represents the data from one mouse. *P < 0.05, **P < 0.01, ***P < 0.005.