These results reinforced the dual role of GPR43 in mediating the proper immune response against Kp. We hypothesize that, in early time points, acetate stimulates neutrophils recruitment and activation in vivo assuring the killing of bacteria, and on the other hand, later during the infection, acetate contributes to the resolution of pulmonary inflammation/injury probably by diminishing neutrophil survival by the increase of IL-10 production (22). Here, FFAR2 is linked to inflammation.