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Amar, N.

Publications and source records attributed to Amar, N..

2 recordsLinked to original sources

Serotype specific anti-capsular polysaccharide IgG associated with colonizing and invasive group B streptococcus in pregnant woman-newborn dyads

Maternal IgG against group B streptococcus (GBS) capsular polysaccharide (CPS), is the principal placental mediator of neonatal protection, yet naturally acquired anti-CPS immunity has not been characterized in North African populations. To address this gap, we conducted a prospective study in a Moroccan mother-newborn cohort to quantify the serotype-specific anti-CPS IgG levels in relation to colonizing versus invasive GBS serotypes. Additionally, we assessed the transplacental transfer of anti-CPS IgG and identified potential correlates of invasive disease. We examined serotype-specific anti-CPS IgG (serotypes Ia-V) in the plasma from maternal and cord blood of 103 GBS-colonized pregnant women, 35 uncolonized controls and their paired newborns (90 paired colonized dyads, including five newborns with invasive GBS disease) using a standardized six-plex immunoassay. Transfer ratios were compared with 1.0 and cord concentrations with published serotype- and onset-specific risk-reduction thresholds. Maternal anti-CPS IgG concentrations varied by serotype, with the highest median for serotype II(1.36g/mL) and the lowest for serotype Ib(0.003g/mL). They were higher in GBS-colonized than uncolonized mothers for serotypes Ia, Ib and II. Maternal and cord blood IgG concentrations were correlated across serotypes, but placental transfer was incomplete, with median ratios of 0.50-0.80. Among 77 newborns, 13.0%(n=10) reached early-onset and 44.2%(n=34) achieved late-onset disease risk-reduction thresholds. The serotype IV was the most identified among neonatal infection disease cases, and this was associated with sub-protective anti-serotype IV antibody. This suggests that while naturally acquired anti-serotype II antibodies were predominant, the low level of anti-serotype IV antibodies could contribute to neonatal infection diseases in mother-newborn pairs.

immunology↗

CD300LG is a receptor for triglyceride-rich lipoproteins that facilitates postprandial lipid clearance

Circulating triglycerides are principally transported by triglyceride-rich lipoprotein particles (TRLs) including very-low-density-lipoproteins (VLDL) and chylomicrons and require the activity of lipoprotein lipase for appropriate lipid processing and cellular uptake. Despite known genetic links between CD300LG variants and altered lipid profiles, the functional role of CD300LG in lipid metabolism remains unclear. In this study, we identify CD300LG as a crucial receptor for TRLs. Human genetic analyses reveal that reduced CD300LG protein levels are causally linked with CAD risk and increased number, diameter, and TAG concentration of TRLs. In mice, CD300LG deficiency results in postprandial hypertriglyceridemia independent of changes in VLDL secretion, intestinal lipid absorption, or lipoprotein lipase activity. Mechanistically, CD300LG acts as a receptor for TRLs through a direct interaction with ApoA4 to facilitate TRL clearance at the microvascular endothelium. These findings elucidate new functions for both CD300LG and ApoA4 and advance our general understanding of triglyceride metabolism.

physiology↗