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Exposure to silver nanoparticles (AgNP) used in consumer products carries potential health risks including increased susceptibility to infectious pathogens. Systematic assessments of antimicrobial macrophage immune responses in the context of AgNP exposure are important because uptake of AgNP by macrophages may lead to alterations of innate immune cell functions. In this study we examined the effects of exposure to AgNP with different particle sizes (20 and 110 nm diameters) and surface chemistry (citrate or polyvinlypyrrolidone capping) on cellular toxicity and innate immune responses against  Mycobacterium tuberculosis  ( M . tb ) by human monocyte-derived macrophages (MDM). Exposures of MDM to AgNP significantly reduced cellular viability, increased  IL8  and decreased  IL10  mRNA expression. Exposure of  M . tb -infected MDM to AgNP suppressed  M . tb -induced expression of  IL1B ,  IL10 , and  TNFA  mRNA. Furthermore,  M . tb -induced IL-1β, a cytokine critical for host resistance to  M . tb , was inhibited by AgNP but not by carbon black particles indicating that the observed immunosuppressive effects of AgNP are particle specific. Suppressive effects of AgNP on the  M . tb -induced host immune responses were in part due to AgNP-mediated interferences with the TLR signaling pathways that culminate in the activation of the transcription factor NF-κB. AgNP exposure suppressed  M . tb -induced expression of a subset of NF-κB mediated genes ( CSF2 ,  CSF3 ,  IFNG ,  IL1A ,  IL1B ,  IL6 ,  IL10 ,  TNFA ,  NFKB1A ). In addition, AgNP exposure increased the expression of  HSPA1A  mRNA and the corresponding stress-induced Hsp72 protein. Up-regulation of Hsp72 by AgNP can suppress  M . tb -induced NF-κB activation and host immune responses. The observed ability of AgNP to modulate infectious pathogen-induced immune responses has important public health implications.

Modulation of Human Macrophage Responses to Mycobacterium tuberculosis by Silver Nanoparticles of Different Size and Surface Modification