Removes the secondary (acyloxyacyl-linked) fatty acyl chains from the lipid A region of bacterial lipopolysaccharides (LPS) (PubMed:12810692, PubMed:15155618, PubMed:17322564, PubMed:19860560). By breaking down LPS, terminates the host response to bacterial infection and prevents prolonged and damaging inflammatory responses (PubMed:17322564, PubMed:19860560, PubMed:28622363). In peritoneal macrophages, seems to be important for recovery from a state of immune tolerance following infection by Gram-negative bacteria (PubMed:18779055). a 3-(acyloxy)acyl derivative of bacterial toxin + H2O = 3-hydroxyacyl derivative of bacterial toxin + a fatty acid + H(+) Binds 3 Ca(2+) ions per subunit. The calcium ions probably have a structural role. Heterodimer of the large and small subunits; disulfide-linked. Detected in urine. Detected in peritoneal macrophages (at protein level) (PubMed:17322564, PubMed:28622363). Strongly expressed in kidney cortex, where it may be produced by proximal tubule cells (PubMed:15155618). In liver, expressed at high levels in Kupffer cells (PubMed:17322564). Expressed by dendritic cells (PubMed:12810692). Detected at low levels in alveolar macrophages (PubMed:28622363). Strongly up-regulated in alveolar macrophages in response to bacterial lipopolysaccharides (LPS). Cleaved into a large and a small subunit. The small subunit is N-glycosylated. Animals develop significant and prolonged hepatosplenomegaly in response to bacterial lipopolysaccharide (LPS) challenge (PubMed:17322564). Both liver and spleen show increased accumulation of leukocytes (PubMed:17322564). Significantly reduced deacylation of LPS in liver and spleen, in peritoneal macrophages, and in bone marrow-derived dendritic cells (PubMed:12810692, PubMed:17322564, PubMed:18779055). Increased lung injury, delayed neutrophil clearance, and prolonged recovery time in response to intranasal LPS administration (PubMed:28622363). Alveolar macrophages show persistent activation and cytokine levels in lung remain elevated 4-7 days after LPS administration (PubMed:28622363). Impaired response to a second infection challenge, with reduced production of the pro-inflammatory chemokines CCL5/RANTES, TNF and IL6 by peritoneal macrophages and reduced survival rates, indicating a prolonged state of immune tolerance (PubMed:18779055). This immune tolerant state can perisist for two months or longer (PubMed:18779055).