Dietary protein and its metabolites, amino acids are essential nutrients for human and animals. Accumulated researches revealed that the gut microbiota mediate the crosstalk between protein metabolism and host immune response. Gut microbes are involved in the digestion, absorption, metabolism and transformation process of dietary protein in the gastrointestinal tract. Amino acids can be metabolized into numerous microbial metabolites, and these metabolites participate in various physiological functions related to host health and diseases. The components of dietary protein impact the gut microbiome composition and microbial metabolites. The source, concentration, and amino acid balance of dietary protein are primary factors which contribute to the composition, structure and function of gut microbes. A suitable ratio between protein and carbohydrate or even a low protein diet is recommended over a diet with protein in excess of requirements. Greater levels and undigested protein lead to an increase of pathogenic microorganism with associated higher risk of metabolic diseases. Herein, the crosstalk between dietary protein and gut microbiome composition and function is summarized, which will help to reveal the potential mechanism of gut microbes on the gastrointestinal tract health.

Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by chronic and relapsing inflammation within the gastrointestinal tract. Antibiotics have been used to treat IBD, primarily utilizing metronidazole. Although there does seem to be a treatment effect, the broad-spectrum antibiotics that have been used to date are crude tools and have many adverse effects. Available evidence suggests that the host microbiome is implicated in the pathogenesis of IBD, though the key bacteria remain unknown. If the bacterial population can be modified appropriately, the use of antibiotics will have a better therapeutic effect. In this study, mice were fed dextran sodium sulfate (DSS) solution for 5 days, followed by 5 days of normal drinking water, to investigate the gut microbiota response to colitis and the initial alteration of microbiota in recovery phase. Day 0 was considered the normal control, while day 5 and day 10 were considered the colitis mouse model progressive phase and recovery phase, respectively. Results showed that inflammation could induce proportional changes in the gut microbiota. Furthermore, transplanting the microbiota in progressive phase to antibiotic-induced microbiota-depleted mice could induce inflammation similar to colitis, which proves the importance of initial alteration of the microbiota for IBD recovery and the potential of the microbiota as a target for the treatment of IBD. Meanwhile, we have also identified three possible target microorganisms in the development of colitis, namely genera Muribaculaceae (negative correlation), Turicibacter (positive correlation) and Lachnospiraceae (negative correlation) in inflammation status through comprehensive analysis.

Human gut Bacteroides and Parabacteroides species play crucial roles in human health and are known for their capacity to utilize diverse polysaccharides. Understanding how these bacteria utilize medicinal polysaccharides is foundational for developing polysaccharides-based prebiotics and drugs. Here, we systematically mapped the utilization profiles of 20 different medicinal polysaccharides by 28 human gut Bacteroides and Parabacteroides species. The growth profiles exhibited substantial variation across different bacterial species and medicinal polysaccharides. Ginseng polysaccharides promoted the growth of multiple Bacteroides and Parabacteroides species; in contrast, Dendrobium polysaccharides selectively promoted the growth of Bacteroides uniformis. This distinct utilization profile was associated with genomic variation in carbohydrate-active enzymes, rather than monosaccharides composition variation among medicinal polysaccharides. Through comparative transcriptomics and genetical manipulation, we validated that the polysaccharide utilization locus PUL34_Bu enabled Bacteroides uniformis to utilize Dendrobium polysaccharides (i.e. glucomannan). In addition, we found that the GH26 enzyme in PUL34_Bu allowed Bacteroides uniformis to utilize multiple plant-derived mannan. Overall, our results revealed the selective utilization of medicinal polysaccharide by Bacteroides and Parabacteroides species and provided insights into the use of polysaccharides in engineering the human gut microbiome.

The gut microbiota plays a critical role in various physiologic processes; however, maternal microbial and metabolic changes during pregnancy and lactation remain elusive. Using pigs as an animal model, we conducted comparative analyses of gut microbiota and short‐chain fatty acid (SCFA) profiles across different stages of gestation, lactation, and the empty (nonpregnancy) phase in 2 distinct breeds of sow, Rongchang (RS) and Landrace (LS). Coriobacteriaceae were found to gradually increase over gestational time irrespective of breed, which was further validated in an independent cohort of sows, indicating that Coriobacteriaceae are likely associated with the progression of pregnancy. Escherichia increased as well. Relative to empty and gestation, lactation was associated with an increase in SCFA producers and a concomitant augmentation in SCFA production in both breeds. A comparison between the 2 breeds revealed that Ruminococcaceae were more abundant in RSs than in LSs, consistent with the strong ability of Rongchang pigs to digest highly fibrous feedstuffs. Taken together, we revealed characteristic structural and metabolic changes in maternal gut microbiota throughout pregnancy, lactation, and the empty phase, which could potentially help improve the pregnancy and lactation outcomes for both animals and humans.—Liu, H., Hou, C., Li, N., Zhang, X., Zhang, G., Yang, F., Zeng, X., Liu, Z., Qiao, S. Microbial and metabolic alterations in gut microbiota of sows during pregnancy and lactation. FASEB J. 33, 4490–4501 (2019). www.fasebj.org

Modulation of the synthesis of endogenous host defense peptides (HDPs) by probiotics represents a novel antimicrobial approach for disease control and prevention, particularly against antibiotic-resistant infections in human and animals. However, the extent of HDP modulation by probiotics is species dependent and strain specific. In the present study, The porcine small intestinal epithelial cell line (IPEC-J2) cells and neonatal piglets were used as in-vitro and in-vivo models to test whether Lactobacillus reuteri I5007 could modulate intestinal HDP expression. Gene expressions of HDPs, toll-like receptors, and fatty acid receptors were determined, as well as colonic short chain fatty acid concentrations and microbiota. Exposure to 10⁸ colony forming units (CFU)/mL of L. reuteri I5007 for 6 h significantly increased the expression of porcine β-Defensin2 (PBD2), pBD3, pBD114, pBD129, and protegrins (PG) 1-5 in IPEC-J2 cells. Similarly, L. reuteri I5007 administration significantly increased the expression of jejunal pBD2 as well as colonic pBD2, pBD3, pBD114, and pBD129 in neonatal piglets (p < 0.05). This was probably associated with the increase in colonic butyric acid concentration and up-regulating expression of Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and G Protein-Coupled Receptor 41 (GPR41) (p < 0.05), but not with stimulation of Pattern-Recognition Receptors. Additionally, supplementation with L. reuteri I5007 in the piglets did not affect the colonic microbiota structure. Our findings suggested that L. reuteri I5007 could modulate intestinal HDP expression and improve the gut health of neonatal piglets, probably through the increase in colonic butyric acid concentration and the up-regulation of the downstream molecules of butyric acid, PPAR-γ and GPR41, but not through modifying gut microbiota structure.

Poison of intestinal induce severe health problems in human infants and young animals due to contaminating foods and feedstuffs. With the emergence of public health concerns and high-speed diffuse of drug-opposition of bacteria, the adoption of antimicrobial peptides as potential candidates in treating pathogen infections raised up. Nature Microcin J25 (MccJ25), a class of lasso peptides separated from a fecal strain of E. coli, has been replied to display powerful antimicrobial behavior. Herein, the study was to assess the usefulness of biogenic MccJ25 in the prophylaxis of ETEC K88 infection in IPEC-J2 cells. In vitro antimicrobial activity against ETEC K88 and cytotoxicity of biogenic MccJ25 were determined first. To further understand how biogenic MccJ25 mediates its impact, ETEC K88 adhesion in cells, membrane permeability [as indicated by reduced release of lactate dehydrogenase (LDH)], transepithelial electrical resistance (TEER), barrier function, and proinflammatory cytokines levels were determined in IPEC-J2 cells after treatment with biogenic MccJ25 and challenge with ETEC K88. Biogenic MccJ25 had a minimum inhibitory concentration of 0.25 μg/mL against ETEC K88, decreased ETEC K88 adhesion in cells and did not cause cytotoxicity toward cells. Furthermore, biogenic MccJ25 protects against ETEC-induced barrier dysfunction by increasing the TEER, decreasing the LDH and promoting tight junction proteins (TJPs) by promoting the assembly of occludin and claudin-1 in the tight junction complex. Biogenic MccJ25 was further found to relieve inflammation responses through modulation of interleukine-6, IL-8 and tumor necrosis factor-α levels via inhibition of mitogen-activated protein kinase (MAPK) and nuclear factor κB activation. In summary, biogenic MccJ25 can protects against ETEC K88-induced intestinal damage and inflammatory response, recommend the hidden adoption of biogenic MccJ25 as a novel prophylactic agent to reduce pathogen infection in animals, food or humans.