15-epi-LXAA4 analog potently inhibits allergen-driven airway hypersensitivity and inflammation in a mouse model. At higher concentrations (>30 nmole/liter), LXA4 binds to AHR, the arylhydrocarbon receptor; following this binding, AHR enters the nucleus, where it joins with AhR nuclear translocator (ARNT). The AHR/ARNT complex binds to xenobiotic response elements to activate transcription of genes, most of which are involved primarily in xenobiotic metabolism. These genes include SOCS2 (i.e. suppressor of cytokine signaling 2), CYP1A1, CYP1A2, CYP1B1, glutathione S-transferase Ya subunit, quinone oxidoreductase, UDP-glucuronosyltransferase and Aldehyde dehydrogenase 3 family, member A1. This LXA4 activity has been demonstrated only in murine cells. LXA4 binds to and activates estrogen receptor alpha. In this capacity, it mimics an estrogenic molecule to stimulate human endometrial epithelial cells in vitro and mouse uterine tissue in vivo. The actions of LXB4 and 15-epi-LXB4 have been far less well defined than those of their LXA4 analogs. Their mechanism of stimulating target cells (e.g. receptors) is not known. One or both of these analogs have been shown to inhibit the recruitment of neutrophils to sites of inflammation, inhibit the cytotoxicity of NK cells, stimulate the recruitment of monocytes to inflammatory sites, enhance macrophage phagocytosis, and suppress the perception of inflammatory pain in rodents. Animal model studies Noninfectious inflammation One or more of the lipoxins or their metabolically resistant analogs have been demonstrated to suppress, limit severity, and/or increase survival in a wide range of inflammatory and allergic diseases as evaluated in mouse and rat model studies. These studies include models of experimentally evoked: Endometriosis , colitis, peritonitis; pancreatitis; kidney inflammation and glomerulonephritis; lung asthma, acid-induced lung injury, cystic fibrosis, pleurisy, brain inflammation and the inflammatory component of Alzheimer's disease; vascular ischemia-reperfusion injuries to various organs including the heart and hind limb; allograph Transplant rejection of heart, kidney, and bone marrow; arthritis; dermatitis; periodontitis; cornea inflammation; and inflammation-based pain and hyperalgesia. Infection-related inflammation Lipoxins have protective effects in animal models of infection-based inflammation: a) LXA4 and a LXA4 analog decreased systemic inflammation and improved survival in rat models of Gram-negative bacterial sepsis; b) 15-epi-LXA4 suppressed the lung injury (i.e., shock lung or Acute respiratory distress syndrome) caused by intraperitoneal injection of Escherichia coli in mice; c) transgenic mice made deficient in lipoxin synthesis by deletion of their Alox5 gene were more susceptible to the inflammatory and lethal effects of Toxoplasma gondii and were rescued from these defects by LXA44; d) LXA4