A cross-sectional study evidences regulations of leukocytes in the colostrum of mothers with obesity.

BACKGROUND: Breastmilk is a dynamic fluid whose initial function is to provide the most adapted nutrition to the neonate. Additional attributes have been recently ascribed to breastmilk, with the evidence of a specific microbiota and the presence of various components of the immune system, such as cytokines and leukocytes. The composition of breastmilk varies through time, according to the health status of mother and child, and altogether contributes to the future health of the infant. Obesity is a rising condition worldwide that creates a state of systemic, chronic inflammation including leukocytosis. Here, we asked whether colostrum, the milk produced within the first 48 h post-partum, would contain a distinct leukocyte composition depending on the body mass index (BMI) of the mother. METHODS: We collected peripheral blood and colostrum paired samples from obese (BMI > 30) and lean (BMI < 25) mothers within 48 h post-partum and applied a panel of 6 antibodies plus a viability marker to characterize 10 major leukocyte subpopulations using flow cytometry. RESULTS: The size, internal complexity, and surface expression of CD45 and CD16 of multiple leukocyte subpopulations were selectively regulated between blood and colostrum irrespective of the study groups, suggesting a generalized cell-specific phenotype alteration. In obesity, the colostrum B lymphocyte compartment was significantly reduced, and CD16+ blood monocytes had an increased CD16 expression compared to the lean group. CONCLUSIONS: This is the first characterization of major leukocyte subsets in colostrum of mothers suffering from obesity and the first report of colostrum leukocyte subpopulations in Latin America. We evidence various significant alterations of most leukocyte populations between blood and colostrum and demonstrate a decreased colostrum B lymphocyte fraction in obesity. This pioneering study is a stepping stone to further investigate active immunity in human breastmilk.

Genome sequences of 70 multidrug-resistant Gram-negative isolates in high-risk neonates in the Northeast of Mexico.

Infections by multidrug-resistant pathogens are steadily increasing worldwide. A considerable proportion of neonatal intensive care admissions have a bacterial infection with multidrug-resistant bacteria during their hospital stay. In this work, we report draft genome sequences of 70 selected isolates from high-risk neonates in the Northeast of Mexico.

Aquaporine-5 and epithelial sodium channel ß-subunit gene expression in gastric aspirates in human term newborns.

Both transient tachypnea of the newborn and neonatal respiratory distress syndrome have been associated with changes in gene expression of aquaporine-5 (AQP5) and the ß subunit of the epithelial sodium channel (ß-ENaC) in the respiratory epithelium. Gastric aspirate (GA) obtained immediately after birth could represent a new source for gene expression analysis for these respiratory diseases. The aims of this study were to determine the feasibility of estimating AQP5 and ß-ENaC gene expression in exfoliated respiratory epithelial cells from the GA of term neonates, and to compare the values with those found in scraped nasal epithelial cells, previously validated as a surrogate for distal lung epithelium in terms of ionic channel activity. The study had a cross-sectional, proof-of-concept design. Immediately after birth, we obtained GA and nasal mucous membrane scrapings from term newborns, in which total RNA and RT-qPCR assays for AQP5 and ß-ENaC genes were performed. AQP5 gene expression was greater in GA than in nasal scrapings, and ß-ENaC gene expression was at least as great in GA as that obtained in nasal scrapings. Amplification of samples from the two sites was comparable. AQP5 gene expression was greater in babies delivered by cesarean section; ß-ENaC gene expression was greater in babies delivered vaginally, but only in the nasal samples. Quantitation of the expression of AQP5 and of ß-ENaC genes in GA, obtained shortly after birth from term newborns is feasible. If confirmed in preterm neonates, this approach could aid in the differential diagnosis of neonatal respiratory diseases.

Can sTREM-1 predict septic shock & death in late-onset neonatal sepsis? A pilot study.

BACKGROUND AND OBJECTIVES: The transmembrane glycoprotein TREM-1 triggers an inflammatory response. Its soluble fraction (sTREM-1) has been shown to have diagnostic accuracy for late-onset neonatal sepsis (LONS). Until now, the potential of sTREM-1 to predict septic shock and/or death in septic neonates has not been explored. This study obtained estimates of the incidence and prevalence of septic shock and/or death in septic neonates for future sample size calculations for confirmatory studies and evaluated the feasibility of using sTREM-1 as a predictor of septic shock and/or death in neonates with LONS criteria. STUDY DESIGN: A pilot study with a cross-sectional design was performed from May 1(st) to October 31(st), 2012. The participants were hospitalized neonates who, after three days of life, were diagnosed as having LONS. Plasma sTREM-1 was quantified by ELISA. The main outcome measurement was the development of septic shock and/or death. RESULTS: Of 71 eligible subjects, nine (12.7%) progressed to septic shock and/or death. In the LONS-Non-Shock group, the sTREM-1 median and interquartile range (IQR) plasma value were 10 (10 to 70) pg/mL. In the LONS & Shock/Death group, the values were 567 (260 to 649) pg/mL. These values were significantly different (Mann-Whitney's U test, p=0.001). A ROC curve for a proposed sTREM-1 cut-off value of 300 pg/mL exhibited an area under the curve of 0.884 (95% CI=0.73 to 1.0; p<0.0001), with a sensitivity of 0.78 (95% CI=0.46 to 0.94) and specificity of 0.97 (95% CI=0.92 to 0.99); PPV would be 0.78 (95% CI=0.46 to 0.94) and NPV 0.97 (95% CI=0.92 to 0.99). CONCLUSIONS: In neonates with LONS, sTREM-1 has the potential to provide an excellent predictive value for septic shock/death. Larger sample sizes are needed to identify the optimal cut-off value of plasma sTREM-1 for this diagnosis and to provide diagnostic accuracy measures.