Microencapsulated Lactobacillus plantarum promotes intestinal development through gut colonization of layer chicks

The effects of Lactobacillus plantarum in microencapsulation(LPM)on intestinal development in layer chicks were investigated in this study,as well as the colonization of L.plantarum in the gut.A total of 480 healthy Hy-Line Brown layer chicks at 0 d old were randomly divided into 4 groups(8 replicates each treatment),and the diets of these birds were supplemented with nothing(control),L.plantarum(0.02 g/kg feed;109 CFU/kg feed),LPM(1.0 g/kg feed;109 CFU/kg feed)and wall material of LPM(WM;0.98 g/kg feed),respectively.Compared to control,LPM improved growth performance and intestinal development of layer chicks,evidenced by significantly increased body weight,average daily gain,average daily feed intake,villus height,villus height/crypt depth,as well as weight and length of the duodenum,jejunum and ileum(P<0.05).These results could be attributed to the increased colonization of L.plantarum in the gut,which was verified by significant increases in lactic acid content,viable counts in chyme and mucosa(P<0.05),as well as a visible rise in number of strains labeled with fluorescein isothiocyanate.Meanwhile,the relative abundances of Lactobacillus and Bifidobacterium significantly increased in response to microencapsulated L.plantarum supplementation(P<0.05),accompanied by the significant up-regulation of colonization related genes(P<0.05),encoding solute carrier family,monocarboxylate transporter,activin A receptor,succinate receptor and secretogranin II.To sum up,microencapsulated L.plantarum supplementation promoted intestinal development,which could be attributed to the enhancement of L.plantarum colonization in the intestine through the mutual assistance of Bifidobacterium and interactions with colonization related transmembrane proteins.

Light-triggered NO-releasing nanoparticles for treating mice with liver fibrosis

Liver fibrosis, resulting from chronic liver damage and characterized by the accumulation of extracellular matrix (ECM) proteins, is a characteristic of most types of chronic liver diseases. The activation of hepatic stellate cells (HSC) is considered an essential pathological hallmark in liver fibrosis. Although nitric oxide (NO) can effectively induce HSC apoptosis, the systemic administration of NO is ineffective and may cause severe complications such as hypotension. To overcome this limitation, nanoparticles were designed to target HSCs and release NO locally under the exposure of near infrared light (NIR). To achieve this, upconversion nanoparticle (UCNP) cores were enveloped in mesoporous silica shells (UCNP@mSiO2), which were modified with hyaluronic acid (HA-UCNP@mSiO2) and Roussin’s black salt (RBS). HA molecules recognize and bind to CD44 proteins, which are overexpressed on activated HSCs. Under exposure to a 980-nm NIR laser, the UCNP cores convert the 980-nm wavelength into ultraviolet (UV) light, which then energizes the RBS (NO donors), resulting in an efficient release of NO inside of the HSCs. Once released, NO triggers HSC apoptosis and reverses the liver fibrosis. This targeted and controlled release method provides the theoretical and experimental basis for novel therapeutic approaches to treat hepatic fibrosis.