Abstract
Long-term colonic inflammation promotes carcinogenesis and histological abnormalities of the liver, and colorectal tumours frequently arise in a background of dysplasia, a precursor of adenomas. Altered colonic microbiota with an increased proportion of bacteria with pro-inflammatory characteristics, have been implicated in neoplastic progression. The composition of the microbiota can be modified by dietary components such as probiotics, polyphenols and dietary fibres. In the present study, the influence of probiotics in combination with blueberry husks on colorectal carcinogenesis and subsequent liver damage was evaluated.Colorectal tumours were induced in rats by cyclic treatment with dextran sulphate sodium (DSS). Blueberry husks and a mixture of three probiotic strains (Bifidobacterium infantis DSM 15159, Lactobacillus gasseri, DSM 16737 and Lactobacillus plantarum DSM 15313) supplemented a basic diet fortified with oats. The condition of the rats was monitored using a disease activity index (DAI). A qualitative and quantitative histological judgement was performed on segments of distal colon and rectum and the caudate lobe of the liver. The formation of short-chain fatty acids, bacterial translocation, the inflammatory reaction and viable count of lactobacilli and Enterobaceriaceae were addressed.Blueberry husks with or without probiotics significantly decreased DAI, and significantly reduced the number of colonic ulcers and dysplastic lesions. With a decreased proportion of blueberry husk in the diet, the probiotic supplement was needed to achieve a significant decrease in numbers of dysplastic lesions. Probiotics decreased faecal viable count of Enterobacteriaceae and increased that of lactobacilli. Blueberry husks with or without probiotics lowered the proportion of butyric acid in distal colon, and decreased the haptoglobin levels. Probiotics mitigated hepatic injuries by decreasing parenchymal infiltration and the incidence of stasis and translocation. The results demonstrate a dietary option for use of blueberry husks and probiotics to delay colonic carcinogenesis and hepatic injuries in the rat model.
Highlights
Cancers may arise from sites of infection, chronic irritation and inflammation [1] and the degree and extent of inflammation during, for example, ulcerative colitis (UC), is a critical component of tumour development and progression [2]
The feed intake was similar for all groups, and all animals gained weight with time, and at the end there were no significant differences between the groups, irrespective of the approach of calculation, i.e. the body weight change (g/animal) was for the C group 173.5 g (167.0–217.5), P group 194.5 g (158.0–217.5), 2B group 173.5 g (149.0–211.5), 2BP group 181.5 g (173.5–204.0), B group 153.0 g (138.0–211.0), blueberry husks and probiotics (BP) group 163.0 g (146.5–196.5), and body weight change in relation to amount of consumed food (g/kg feed/animal) was for the C group 56.0 g (53.9–70.2), P group 62.7 g (51.0–70.2), 2B group 54.2 g (46.6–66.1), 2BP group 55.0 g (52.6–61.8), B group (47.8 g (43.1– 65.9), BP group 54.3 g (48.8–65.5)
The signs of colitis gradually disappeared during the first periods with pure water, but disease activity index (DAI) gradually increased over time and did not revert between the cycles of dextran sulphate sodium (DSS) administration (Fig. 1)
Summary
Cancers may arise from sites of infection, chronic irritation and inflammation [1] and the degree and extent of inflammation during, for example, ulcerative colitis (UC), is a critical component of tumour development and progression [2]. The cause of gastrointestinal tumours is implicating chronic inflammation in response to an adverse bacterial flora as a promotion of neoplastic progression, and the intestinal environment is considered important in both colorectal cancer development and modulation of mucosal immunity [7]. During inflammation in UC-patients, different members of the Enterobacteriaceae family and different Clostridium species have been found to increase in accordance with a decrease in bifidobacteria and lactobacilli [8,9]. This change in the composition of the microbiota, leading to an imbalance between potentially beneficial and adverse bacteria, can contribute to the pathogenesis. Translocated LPS can cause extensive damage to a variety of organs, including the liver [11]
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