Preparation and characterization of standard reference material 1849 infant/adult nutritional formula.

Standard Reference Material (SRM) 1849 Infant/Adult Nutritional Formula has been issued by the National Institute of Standards and Technology (NIST) as a replacement for SRM 1846 Infant Formula, issued in 1996. Extraction characteristics of SRM 1846 have changed over time, as have NIST's analytical capabilities. While certified mass fraction values were provided for five constituents in SRM 1846 (four vitamins plus iodine), certified mass fraction values for 43 constituents are provided in SRM 1849 (fatty acids, elements, and vitamins) and reference mass fraction values are provided for an additional 43 constituents including amino acids and nucleotides, making it the most extensively characterized food-matrix SRM available from NIST.

Involvement of TLR2 and TLR4 in inflammatory immune responses induced by fine and coarse ambient air particulate matter.

Induction of proinflammatory mediators by alveolar macrophages exposed to ambient air particulate matter has been suggested to be a key factor in the pathogenesis of inflammatory and allergic diseases in the lungs. However, receptors and mechanisms underlying these responses have not been fully elucidated. In this study, we examined whether TLR2, TLR4, and the key adaptor protein, MyD88, mediate the expression of proinflammatory cytokines and chemokines by mouse peritoneal macrophages exposed to fine and coarse PM. TLR2 deficiency blunted macrophage TNF-alpha and IL-6 expression in response to fine (PM2.5), while not affecting cytokine-inducing ability of coarse NIST Standard Reference Material (SRM 1648) particles. In contrast, TLR4(-/-) macrophages showed inhibited cytokine expression upon stimulation with NIST SRM 1648 but exhibited normal responses to PM2.5. Preincubation with polymyxin B markedly suppressed the capacity of NIST SRM 1648 to elicit TNF-alpha and IL-6, indicating endotoxin as a principal inducer of cytokine responses. Overexpression of TLR2 in TLR2/4-deficient human embryonic kidney 293 cells imparted PM2.5 sensitivity, as judged by IL-8 gene expression, whereas NIST SRM 1648, but not PM2.5 elicited IL-8 expression in 293/TLR4/MD-2 transfectants. Engagement of TLR4 by NIST SRM 1648 induced MyD88-independent expression of the chemokine RANTES, while TLR2-reactive NIST IRM PM2.5 failed to up-regulate this response. Consistent with the shared use of MyD88 by TLR2 and TLR4, cytokine responses of MyD88(-/-) macrophages to both types of air PM were significantly reduced. These data indicate differential utilization of TLR2 and TLR4 but shared use of MyD88 by fine and coarse air pollution particles.