Binding of Human Milk to Pathogen Receptor DC-SIGN Varies with Bile Salt-Stimulated Lipase (BSSL) Gene Polymorphism

OBJECTIVE: Dendritic cells bind an array of antigens and DC-SIGN has been postulated to act as a receptor for mucosal pathogen transmission. Bile salt-stimulated lipase (BSSL) from human milk potently binds DC-SIGN and blocks DC-SIGN mediated trans-infection of CD4(+) T-lymphocytes with HIV-1. Objective was to study variation in DC-SIGN binding properties and the relation between DC-SIGN binding capacity of milk and BSSL gene polymorphisms. STUDY DESIGN: ELISA and PCR were used to study DC-SIGN binding properties and BSSL exon 11 size variation for human milk derived from 269 different mothers distributed over 4 geographical regions. RESULTS: DC-SIGN binding properties were highly variable for milks derived from different mothers and between samplings from different geographical regions. Differences in DC-SIGN binding were correlated with a genetic polymorphism in BSSL which is related to the number of 11 amino acid repeats at the C-terminus of the protein. CONCLUSION: The observed variation in DC-SIGN binding properties among milk samples may have implications for the risk of mucosal transmission of pathogens during breastfeeding

Additional file 1: Figure S3. of Forkhead Box F1 promotes breast cancer cell migration by upregulating lysyl oxidase and suppressing Smad2/3 signaling

FoxF1-induced upregulation of LOX increases invasiveness. An additional siRNA against LOX was used to confirm the effect of LOX depletion on invasive capacity of HC11FoxF1 cells shown in Fig. 3b. A, densitometry of western blot analysis of supernatant with LOX antibody after transfection with LOX siRNA or mock-treatment. B, relative invasion capacity following LOX RNAi. (PDF 286 kb

Additional file 3: Figure S1. of Forkhead Box F1 promotes breast cancer cell migration by upregulating lysyl oxidase and suppressing Smad2/3 signaling

NFI-C2 and FoxF1 regulates expression of genes involved in EMT. Reverse transcription PCR analysis of Desmoglein 1β, Twist1, Zeb1, Snail1 and GAPDH mRNA levesl in parental, NFI-C2- or FoxF1-overexpressing HC11 cells. (PDF 475 kb