A total of 50 weaning pigs (16 d of age; 4.72 +/- 0.23 kg of BW) were selected to investigate the effect of dietary chito-oligosaccharide (COS) supplementation on growth performance, fecal shedding of Escherichia coli and Lactobacillus, apparent digestibility, and small intestinal morphology. Pigs housed in individual metabolic cages were assigned randomly to 5 treatments (n = 10), including 1 basal diet (control), 3 diets with COS supplementation (100, 200, and 400 mg/kg), and 1 diet with chlortetracycline (CTC) supplementation (80 mg/kg). Fresh fecal samples were collected to evaluate shedding of E. coli and Lactobacillus on d 0, 7, 14, and 21 postweaning. Fresh fecal samples collected from each cage from d 19 to 21 were stored frozen for determination of apparent total tract digestibility. On d 21, all pigs were killed to collect the middle sections of the duodenum, jejunum, and ileum for determination of mucosa morphology. Supplementation of COS at 100 and 200 mg/kg and supplementation of CTC improved (P < 0.05) overall ADG, ADFI, and G:F in comparison with the control. Supplementation of COS at 200 mg/kg as well as supplementation of CTC increased (P < 0.05) apparent total tract digestibility of DM, GE, CP, crude fat, Ca, and P, whereas COS at 100 mg/kg increased (P < 0.05) the digestibility of DM, Ca, and P in comparison with the control diet. Pigs receiving diets supplemented with COS or CTC had a decreased (P < 0.05) incidence of diarrhea and decreased diarrhea scores compared with control pigs. Fecal samples from pigs receiving diets supplemented with COS had greater (P < 0.05) Lactobacillus counts than those from control pigs and pigs receiving diets supplemented with CTC on d 14 and 21. However, supplementation of COS at 200 mg/kg and supplementation of CTC decreased (P < 0.05) E. coli counts in the feces on d 21 compared with the control diet. Dietary supplementation of COS at 200 mg/kg and of CTC increased (P < 0.05) the villus height and villus:crypt ratio at the ileum and jejunum, and COS at 100 mg/kg also increased (P < 0.05) the villus height in the ileum compared with the control diet. The current results indicated that dietary supplementation of COS at 100 and 200 mg/kg enhanced growth performance by increasing apparent digestibility, decreasing the incidence of diarrhea, and improving small intestinal morphology.

Lactobacilli represent components of the commensal mammalian gastrointestinal microbiota and are useful as probiotics, functional foods, and dairy products. This study includes systematic polyphasic analyses of murine intestinal Lactobacillus isolates and correlation of taxonomic findings with data from cytokine production assays. Lactobacilli were recovered from mice with microbiota-dependent colitis (interleukin-10 [IL-10]-deficient C57BL/6 mice) and from mice without colitis (Swiss Webster and inducible nitric oxide synthetasedeficient C57BL/6 mice). Polyphasic analyses were performed to elucidate taxonomic relationships among 88 reference and murine gastrointestinal lactobacilli. Genotypic tests included single-locus analyses (16S ribosomal DNA sequencing and 16S-23S rRNA intergenic spacer region PCR) and genomic DNA profiling (repetitive DNA element-based PCR), and phenotypic analyses encompassed more than 50 tests for carbohydrate utilization, enzyme production, and antimicrobial resistance. From 20 mice without colitis, six Lactobacillus species were recovered; the majority of the mice were colonized with L. reuteri or L. murinus (72% of isolates). In contrast, only, L. johnsonii was isolated from 14 IL-10-deficient mice. Using an in vitro assay, we screened murine isolates for their ability to inhibit tumor necrosis factor alpha (TNF-␣) secretion by lipopolysaccharide-activated macrophages. Interestingly, a subpopulation of lactobacilli recovered from mice without colitis displayed TNF-␣ inhibitory properties, whereas none of the L. johnsonii isolates from IL-10-deficient mice exhibited this effect. We propose that differences among intestinal Lactobacillus populations in mammals, combined with host genetic susceptibilities, may account partly for variations in host mucosal responses.