Probably removes the 4'-phosphate group from lipid A. Removal of this phosphate group confers resistance to cationic antimicrobial peptides (CAMPs), inflammation-associated peptides produced by the human host. This LPS modification helps maintain the stability of this commensal bacterium in gut microbiota. Bacterial outer membrane biogenesis; LPS lipid A biosynthesis. No visible phenotype in the absence of host gut inflammation. Loss of resistance to the cationic antimicrobial peptide polymyxin B (PMB). Lipid A is bi- rather than mono-phosphorylated, with mass corresponding to a 1- 4'-phosphorylated molecule. Increased negative charge on the cell surface leading to greater binding of PMB, increased outer membrane disruption by PMB. Decreased survival (fitness) in host (mouse) cells after infection with C.rodentium (a mouse enteropathogen that induces inflammation) or in mice subjected to other inflammation-producing stimuli. In this organism the major lipid A structure is a pentaacylated disaccharide of glucosamine with a single phosphate at the 1- position. Belongs to the lipid A LpxF 4'-phosphatase family.