restored macrophage function caused by respiratory syncytial virus in transgenic mice made deficient of lipoxin synthesis by Alox5 gene deletion; e) LXA4 ameliorated infectious periodontitis in rabbit and porcine models. f) 15-epi-LXA4 decreased parasite blood levels, decrease cardiac inflammation, and increase survival in a mouse model of Trypanosoma cruzi-induced Chagas disease; f)' 15-epi-LXA4 prolonged survival in a mouse model of Plasmodium berghei-induced cerebral malaria; and g) LXA4 shortens the duration of the allergic response to the parasitic infestation, Angiostrongylus costaricensis. However, lipoxins also have harmful effects in these models: aerosol infection with Mycobacterium tuberculosis in transgenic mice defective in ALOX5, which contributes to LX synthesis, exhibited far less severe inflammation and better survival than control mice; and treatment of the transgenic mice with oral LXA4 reversed the protective effect of ALOX5 deletion. Human studies Preclinical studies LXs and epi-LXs have been detected in a various human tissues undergoing a wide range of inflammatory reactions, allergic reactions, and other conditions such as in the blood of patients undergoing coronary angioplasty or strenuous exercise. LXA4 inhibits the-bronchial contracting action of LTC4 and relaxes pre-contracted bronchi in asthmatic individuals. Kaposi's sarcoma-associated herpesvirus (KSHV) causes the malignant transformation of human cells and is responsible for Kaposi's sarcoma and primary effusion lymphoma, two cancers which afflict in particular humans infected with HIV. Studies in human Kaposi sarcoma and primary effusion lymphoma cells find that: a) KSHV promotes the production of pro-inflammatory cytokines, lipoxygenases, cyclooxygenase, and metabolites of the latter two classes of enzymes while suppressing production of anti-inflammatory signaling agents such as LXA4, apparently as a strategy to promote its latency and malignant transforming ability; b)' Kaposi sarcoma and primary effusion lymphoma cells express the ALX/FPR receptor; and c)' treatment of the latter cells with LXA4 or 15-epi-LXA4 reverses this pro-malignancy profile of pro-inflammatory signaling by an ALX/FPR-dependent mechanism. These studies suggest that the two LX's or their analogs should be tested in animal models to determine if the might be useful for treating the two human malignancies. Clinical studies In a randomized controlled trial, topical application of 15-epi-LXA4 or a comparatively stable analog of LXB4, 15R/S-methyl-LXB4, reduced the severity of eczema in a study of 60 infants. Currently, BLXA4, a lipoxin analog, is in clinical trial phase 1 and currently recruiting volunteers for treating oral gingivitis (see: Safety and Preliminary Efficacy of Lipoxin Analog BLXA4-ME Oral Rinse for the Treatment of Gingivitis (BLXA4) at