Pectin alleviates the pulmonary inflammatory response induced by PM2.5 from a pig house by modulating intestinal microbiota

This study aimed to investigate whether dietary fiber pectin can alleviate PM2.5-induced pulmonary inflammation and the potential mechanism. PM2.5 samples were collected from a nursery pig house. The mice were divided into three groups: the control group, PM2.5 group and PM2.5 + pectin group. The mice in the PM2.5 group were intratracheally instilled with PM2.5 suspension twice a week for four consecutive weeks, and those in the PM2.5 + pectin group were subject to the same PM2.5 exposure, but fed with a basal diet supplemented with 5% pectin. The results showed that body weight and feed intake were not different among the treatments (p > 0.05). However, supplementation with pectin relieved PM2.5-induced pulmonary inflammation, presenting as slightly restored lung morphology, decreased mRNA expression levels of IL-1β, IL-6 and IL-17 in the lung, decreased MPO content in bronchoalveolar lavage fluid (BLAF), and even decreased protein levels of IL-1β and IL-6 in the serum (p < 0.05). Dietary pectin altered the composition of the intestinal microbiota, increasing the relative abundance of Bacteroidetes and decreasing the ratio of Firmicutes/Bacteroidetes. At the genus level, short-chain fatty acid (SCFA)-producing bacteria, such as Bacteroides, Anaerotruncus, Prevotella 2, Parabacteroides, Ruminococcus 2 and Butyricimonas, were enriched in the PM2.5 +pectin group. Accordingly, dietary pectin increased the concentrations of SCFAs, including acetate, propionate, butyrate and valerate, in mice. In conclusion, dietary fermentable fiber pectin can relieve PM2.5-induced pulmonary inflammation via alteration of intestinal microbiota composition and SCFA production. This study provides a new insight into reducing the health risk associated with PM2.5 exposure

Asymmetric Coordination Induces Electron Localization at Ca Sites for Robust CO2 Electroreduction to CO

Main group single atom catalysts (SACs) are promising for CO2 electroreduction to CO by virtue of their ability in preventing the hydrogen evolution reaction and CO poisoning. Unfortunately, their delocalized orbitals reduce the CO2 activation to *COOH. Herein, an O doping strategy to localize electrons on p-orbitals through asymmetric coordination of Ca SAC sites (Ca-N3O) is developed, thus enhancing the CO2 activation. Theoretical calculations indicate that asymmetric coordination of Ca-N3O improves electron-localization around Ca sites and thus promotes *COOH formation. X-ray absorption fine spectroscopy shows the obtained Ca-N3O features: one O and three N coordinated atoms with one Ca as a reactive site. In situ attenuated total reflection infrared spectroscopy proves that Ca-N3O promotes *COOH formation. As a result, the Ca-N3O catalyst exhibits a state-of-the-art turnover frequency of ≈15 000 per hour in an H-cell and a large current density of −400 mA cm−2 with a CO Faradaic efficiency (FE) ≥ 90% in a flow cell. Moreover, Ca-N3O sites retain a FE above 90% even with a 30% diluted CO2 concentration