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. 2015 Sep;81(18):6425-35.
doi: 10.1128/AEM.01360-15. Epub 2015 Jul 10.

Attenuation of Colitis by Lactobacillus casei BL23 Is Dependent on the Dairy Delivery Matrix

Bokyung Lee  1 , Xiaochen Yin  1 , Stephen M Griffey  2 , Maria L Marco  3
Affiliations

Attenuation of Colitis by Lactobacillus casei BL23 Is Dependent on the Dairy Delivery Matrix

Bokyung Lee et al. Appl Environ Microbiol. 2015 Sep.

Abstract

The role of the food delivery matrix in probiotic performance in the intestine is not well understood. Because probiotics are often provided to consumers in dairy products, we investigated the contributions of milk to the health-benefiting performance of Lactobacillus casei BL23 in a dextran sulfate sodium (DSS)-induced murine model of ulcerative colitis. L. casei BL23 protected against the development of colitis when ingested in milk but not in a nutrient-free buffer simulating consumption as a nutritional supplement. Consumption of (acidified) milk alone also provided some protection against weight loss and intestinal inflammation but was not as effective as L. casei and milk in combination. In contrast, L. casei mutants deficient in DltD (lipoteichoic acid d-alanine transfer protein) or RecA (recombinase A) were unable to protect against DSS-induced colitis, even when consumed in the presence of milk. Mice fed either L. casei or milk contained reduced quantities of colonic proinflammatory cytokines, indicating that the L. casei DltD(-) and RecA(-) mutants as well as L. casei BL23 in nutrient-free buffer were effective at modulating immune responses. However, there was not a direct correlation between colitis and quantities of these cytokines at the time of sacrifice. Identification of the cecal microbiota by 16S rRNA gene sequencing showed that L. casei in milk enriched for Comamonadaceae and Bifidobacteriaceae; however, the consumption of neither L. casei nor milk resulted in the restoration of the microbiota to resemble that of healthy animals. These findings strongly indicate that probiotic strain efficacy can be influenced by the food/supplement delivery matrix.

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Figures

FIG 1
FIG 1
Survival of L. casei in DSS-treated mice. Viable, rifampin-resistant L. casei cells in mouse stools were enumerated every second day of the study. The average CFU ± standard errors from fecal samples are shown for each treatment and time point (lower limit of detection, 1,000 CFU/g feces). Fecal samples were recovered from nine mice in each group, except for two BL580- and milk-fed mice on days 14 and 15 due to early termination. Because of diarrhea in some animals, stools were collected from the following numbers of mice on days 14 and 15, respectively: 7 and 6 mice fed BL23 and PBS, 6 and 8 mice fed BL23 and milk, 5 and 5 mice fed BL580 and milk, and 9 and 9 mice fed BL180 and milk.
FIG 2
FIG 2
Changes in mouse body weight during and after DSS administration. The percent change in body weight was calculated by using the weight on day 4 (the day of DSS initiation) as the reference. The averages ± standard deviations of data from 12 mice (healthy sham control and DSS treated) and 9 mice (L. casei or acidified milk fed) are shown. **, P < 0.01; ***, P < 0.001 according to the Student t test compared to the DSS control group.
FIG 3
FIG 3
L. casei in milk protects against DSS colitis. Stool consistency (diarrhea) (A), histological scores (B), and disease activity indices (C) were calculated according to the criteria shown in Table 2. A higher score means greater severity. The averages ± standard deviations of data from 12 mice (healthy sham control and DSS treated) and 9 mice (L. casei or acidified milk fed) are shown. *, P < 0.05; ***, P < 0.001 according to the Student t test compared to the DSS control group.
FIG 4
FIG 4
Intestinal cytokine production differs depending on intestinal location, DSS-induced colitis, and consumption of L. casei or milk. (A to C) PCA of cytokine amounts in colonic and ileal tissues (A) and the colon (B) and ileum (C) of healthy (sham) and DSS-treated mice. (D to F) PCA comparisons of cytokine quantities in colonic tissues of healthy (sham) and DSS-treated control mice and DSS-treated mice fed milk with or without BL23 (D), L. casei BL23 in PBS (E), or the L. casei DltD− (BL580) or L. casei RecA− (BL180) strain in milk (F). The numbers of mice and cytokines used for this analysis are listed in Table S1 in the supplemental material.
FIG 5
FIG 5
L. casei regulates cytokine production in colon during DSS-induced colitis. The quantities of IL-1α (A), IL-6 (B), IL-17 (C), KC (D), G-CSF (E), and MCP-1 (F) in colonic tissue were measured. Shown are averages ± standard deviations of data from 12 healthy sham-treated mice; 9 mice treated with DSS alone (control), acidified milk, L. casei BL23 in milk, L. casei in PBS, or L. casei BL180 in milk; and 7 mice fed L. casei BL580 in milk. *, P < 0.05; **, P < 0.01; ***, P < 0.001 according to the Mann-Whitney U test compared to the DSS-treated control group.
FIG 6
FIG 6
Mouse cecal microbiota is altered by DSS, milk, and L. casei. (A) Weighted UniFrac PCoA of the cecal microbiota structure. (B) Taxonomy analysis at the family level. In panel B, the dendrogram on the left shows the Euclidean distance calculated from the bacterial family abundance in each treatment group. The bars on the right indicate the relative abundances of different families with representation of at least 1% in the total DNA sequence reads examined. Asterisks indicate “ unclassified” DNA sequences that are similar to more than one sequence from the reference database and “undefined” sequences that are similar to an unnamed reference sequence.
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