Early life environmental exposures have a minor impact on the gut ecosystem following a natural birth

A growing body of evidence suggests that the environment is an important source of colonizing bacteria for the gastrointestinal tract of C-section delivered infants, who undergo multiple birth-related interventions; however, the extent to which environmental microbes impact vaginally delivered infants remains unclear. Here we investigated the impact of rural and urban environmental exposures on microbial establishment and immunity in vaginally delivered mice. We simulated rural and urban home environments by adding soil types to cages from breeding to weaning. Our aims were to determine the impact of rural and urban soil exposures on the gut microbiome in young mice and to understand whether these changes persisted into adulthood. Host immune cytokines and microbial short-chain fatty acids were quantified to understand the impact on immunity. We found that early-life soil exposure had a minor effect on the richness of the neonatal gut microbiota contributing 5% and 9% variation in the bacterial community structure between mice during early-life and adulthood, respectively. Exposure to urban soil increased Clostridiaceae and propionic acid which persisted into adulthood. While soil exposure had a limited effect on the gut taxa, systemic cytokine and chemokine profiles were altered in adulthood. The findings presented here show that unlike in C-section deliveries previously reported, environmental exposures following a natural birth have a limited impact on the gut microbial taxa but potentially play an important role in immune-mediated disease susceptibility later in life

Fish oil attenuates omega-6 polyunsaturated fatty acid-induced dysbiosis and infectious colitis but impairs LPS dephosphorylation activity causing sepsis.

Clinically, excessive ω-6 polyunsaturated fatty acid (PUFA) and inadequate ω-3 PUFA have been associated with enhanced risks for developing ulcerative colitis. In rodent models, ω-3 PUFAs have been shown to either attenuate or exacerbate colitis in different studies. We hypothesized that a high ω-6: ω-3 PUFA ratio would increase colitis susceptibility through the microbe-immunity nexus. To address this, we fed post-weaned mice diets rich in ω-6 PUFA (corn oil) and diets supplemented with ω-3 PUFA (corn oil+fish oil) for 5 weeks. We evaluated the intestinal microbiota, induced colitis with Citrobacter rodentium and followed disease progression. We found that ω-6 PUFA enriched the microbiota with Enterobacteriaceae, Segmented Filamentous Bacteria and Clostridia spp., all known to induce inflammation. During infection-induced colitis, ω-6 PUFA fed mice had exacerbated intestinal damage, immune cell infiltration, prostaglandin E2 expression and C. rodentium translocation across the intestinal mucosae. Addition of ω-3 PUFA on a high ω-6 PUFA diet, reversed inflammatory-inducing microbial blooms and enriched beneficial microbes like Lactobacillus and Bifidobacteria, reduced immune cell infiltration and impaired cytokine/chemokine induction during infection. While, ω-3 PUFA supplementation protected against severe colitis, these mice suffered greater mortality associated with sepsis-related serum factors such as LPS binding protein, IL-15 and TNF-α. These mice also demonstrated decreased expression of intestinal alkaline phosphatase and an inability to dephosphorylate LPS. Thus, the colonic microbiota is altered differentially through varying PUFA composition, conferring altered susceptibility to colitis. Overall, ω-6 PUFA enriches pro-inflammatory microbes and augments colitis; but prevents infection-induced systemic inflammation. In contrast, ω-3 PUFA supplementation reverses the effects of the ω-6 PUFA diet but impairs infection-induced responses resulting in sepsis. We conclude that as an anti-inflammatory agent, ω-3 PUFA supplementation during infection may prove detrimental when host inflammatory responses are critical for survival

Importance of oxygen in the metal-free catalytic growth of single-walled carbon nanotubes from SiOx by a vapor-solid-solid mechanism

To understand in-depth the nature of the catalyst and the growth mechanism of single-walled carbon nanotubes (SWCNTs) on a newly developed silica catalyst, we performed this combined experimental and theoretical study. In situ transmission electron microscopy (TEM) observations revealed that the active catalyst for the SWCNT growth is solid and amorphous SiO nanoparticles (NPs), suggesting a vapor-solid-solid growth mechanism. From in situ TEM and chemical vapor deposition growth experiments, we found that oxygen plays a crucial role in SWCNT growth in addition to the well-known catalyst size effect. Density functional theory calculations showed that oxygen atoms can enhance the capture of -CH and consequently facilitate the growth of SWCNTs on oxygen-containing SiO NPs

Composition of high-fat diets.

1<p>Mineral mix (mg/g): di calcium phosphate 500, magnesium oxide 24; potassium citrate 220, potassium sulfate 52; sodium chloride 74, chromium KSO₄ 12H₂0 0.55; cupric carbonate 0.3, potassium iodate 0.01; ferric citrate 6, manganous carbonate 3.5, sodium selenite 0.01, zinc carbonate 1.6; sucrose 118.03.</p>2<p>Vitamin Mix (mg/g): vitamin A 0.8; vitamin D₃ 1; vitamin E 10; menadione sodium bisulfite 0.08; nicotinic acid 3; calcium pantothenate 1.6; pyridoxine HCl 0.7; riboflavin 0.6; thiamin 0.6; sucrose 978.42.</p>3<p>Added to meet essential fatty acid requirements for all groups.</p

ω-3 PUFA supplementation to ω-6 PUFA rich diets resulted in impaired infection-induced intestinal alkaline phosphatase activity.

<p>A) IAP+ cells were highest in ω-6 PUFA rich diet groups during infection and ω-3 PUFA supplementation impaired this response. Colon sections were stained for the presence of IAP+ cells and quantified. Representative immunofluorescence images are shown at 200× magnification (scale bar = 13.6 µm). B) While both the low and high ω-6 PUFA rich diet groups showed an induction of LPS-dephosphorylating activity during infection induced colitis, theω-3 PUFA supplementation fed mice were unable to dephosphorylate LPS in response to infection. Colonic tissues were homogenized, supernatant collected and LPS incubated with each diet group for 2 hours. A colorimetric malachite green solution was used to measure absorbance at 620 nm and the LPS-dephosphorylating activity/mg of protein was determined for each diet group. (*, <i>P</i><0.05; **, <i>P</i><0.005).</p

ω-3 PUFA supplementation to ω-6 PUFA rich diets impairs intestinal inflammatory cell infiltration during <i>C. rodentium-</i>induced colitis.

<p>While ω-6 PUFA rich diets induced the infiltration of macrophages, neutrophils and PGE2 inflammatory cells, ω-3 PUFA supplementation prevented the enhanced infiltration during infection. Colon sections were stained for the presence of submucosal A) F4/80+ macrophages B) MPO+ neutrophils and C) PGE2+ cells and quantified. Representative immunofluorescence images are shown at 200× magnification. (scale bar = 13.6 µm; *, <i>P</i><0.05).</p

Major fatty acid compositions of dietary oil used in preparing high-fat diets.

<p>Major fatty acid compositions of dietary oil used in preparing high-fat diets.</p