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Article in English | WPRIM | ID: wpr-819553


OBJECTIVE@#To investigate which life stage of the parasite has the ability to stimulate release of pro- or anti-inflammatory mediators from macrophages.@*METHODS@#The human macrophage/monocyte cell line THP-1, the mouse macrophage cell line RAW 264.7 and naive peritoneal macrophages (PM) from the rodent host Mastomys coucha (M. coucha) were incubated at 37 °C in 5% CO(2) atmosphere with extracts of microfilariae (Mf), third stage infective larvae (L(3)) and adult worms (Ad) of Brugia malayi. After 48 hr post exposure, IL-1β, IL-6, TNF-α, IL-10 and nitric oxide (NO) in cell-free supernatants were estimated.@*RESULTS@#Extracts of all the life stages of the parasite were capable of stimulating pro- (IL-1β, IL-6 and TNF-α) and anti-inflammatory (IL-10) cytokines in both the cell lines and peritoneal macrophages of M. coucha. Mf was the strongest stimulator of pro-inflammatory cytokines followed by L(3) and Ad; however, Ad was a strong stimulator of IL-10 release. Mf was found to have potential to modulate LPS-induced NO release in RAW cells. Ad-induced NO release was concentration dependent with maximum at 20 μg/mL in both RAW and PMs.@*CONCLUSIONS@#The results show that parasites at all life stages were capable of stimulating pro- (IL-1β, IL-6 and TNF-α) and anti-inflammatory (IL-10) cytokines and NO release from macrophages of susceptible host M. coucha, human and mouse macrophage cell lines. Mf can suppress the LPS-induced NO release in RAW cells. The findings also show that the two cell lines may provide a convenient in vitro system for assaying parasite-induced inflammatory mediator release.

Animals , Brugia malayi , Allergy and Immunology , Cells, Cultured , Culture Media , Chemistry , Female , Humans , Inflammation Mediators , Metabolism , Interleukin-10 , Metabolism , Interleukin-1beta , Metabolism , Interleukin-6 , Metabolism , Macrophages, Peritoneal , Allergy and Immunology , Parasitology , Male , Mice , Murinae , Allergy and Immunology , Parasitology , Tumor Necrosis Factor-alpha , Metabolism