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The microbiome and cow’s milk allergy in infants
Feehley T, Plunkett CH, Bao R, et al. Healthy infants harbour intestinal bacteria that protect against food allergy. Nature Medicine 2019. doi: 10.1038/s41591-018-0324-z. [Epub ahead of print 14 Jan 2019].
The gut microbiome differs between healthy infants and those allergic to cow’s milk. In this study, the role of commensal bacteria in allergy was tested using mouse models. Faeces from four healthy infants and four cow’s milk allergic (CMA) infants were transplanted into germ-free mice using intragastric gavage. All infants were formula fed, and mice were given the same formula as infants in addition to mouse chow. After sensitisation, mice were challenged with cow’s milk allergen beta-lactoglobulin (BLG). Control germ-free mice and CMA-colonised mice developed anaphylactic responses, measured by a drop in core body temperature and production of BLG-specific IgE and IgG1. Mice colonised with healthy infant microbiota did not develop anaphylaxis. Analysis of the infant faeces showed a variation in 58 operational taxonomic units between the two groups, and notably, Lachnospiracae was enriched in healthy-colonised mice. Ileal epithelial cells were isolated and sequenced, and there was a difference between the two mouse groups, suggesting that ileal bacteria regulate host responses. The 16S sequence of the Lachnospiracae present in healthy mice matched most closely to Anaerostipes caccae, and this species was enriched in ileal and faecal samples of healthy-colonised mice. A. caccae is an anaerobic butyrate-producing bacterium in the Clostridial class and implicated in protecting against nut allergy. Germ-free mice were monocolonised with A. caccae and were protected against anaphylaxis to the BLG challenge. In summary commensal bacteria play a critical role in regulating allergic responses to food, and the microbiome could be harnessed to prevent and treat food allergy.
STING activation in macrophages drives liver inflammation in NASH
Yu Y, Liu Y, An W, et al. STING-mediated inflammation in Kupffer cells contributes to progression of …
Competing interests None declared.
Provenance and peer review Not commissioned; internally peer reviewed.
Patient consent for publication Not required.
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