Abstract：
:Lead (Pb) alters the susceptibility to different pathogens suggesting that macrophage-mediated defense mechanisms, through activation of toll-like receptors (TLRs), may be affected by Pb. The aim of this study was to test whether activation of TLR4 is a targeted molecule to the effect of environmentally relevant Pb concentrations (0.05, 0.5 and 5μg/dL). The function of macrophages activated through TLR4 was evaluated using as TLR4 ligand lipopolysaccharides (LPSs) from two different pathogens: Escherichia coli and Salmonella typhimurium. Pb induced proliferation, increased the NO(-) baseline, IL-1β and IL-6 secretion. Interestingly, Pb exposure induced differential effects on cells stimulated with the two LPS used: in macrophages stimulated with LPS from E. coli, Pb caused an early decrease in proliferation, increase NO(-) production, and decrease IL-6 and TNF-α secretion; in macrophages stimulated with LPS from S. typhimurium, Pb decreased proliferation after 36h, induced a biphasic effect on NO(-) production, and enhance the secretion of IL-1β, IL-6 and TNF-α. Results suggest that TLR4 is a target for the Pb effect, which up to 5.0μg/dL affect immune competence against pathogens, dependent on the bacterial species. This effect may be attributable to structural differences that determine LPS affinity for TLR4.
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Luna AL,Acosta-Saavedra LC,Martínez M,Torres-Avilés N,Gómez R,Calderón-Aranda ESdoi
10.1016/j.toxlet.2012.09.009subject
Has Abstractpub_date
2012-11-15 00:00:00pages
301-6issue
3eissn
0378-4274issn
1879-3169pii
S0378-4274(12)01305-7journal_volume
214pub_type
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