Gut microbiota has been demonstrated to be involved in intestinal nutrition, defense, and immunity, as well as participating in disease progression. This study was to investigate gut microbiota changes in chickens challenged with netB -positive Clostridium perfringens strain (CP1) and/or the predisposing Eimeria species ( Eimeria ) and fed diets with fishmeal supplementation. In addition, the effects of lauric acid, a medium-chain fatty acid (MCFA), on necrotic enteritis (NE) reduction and modulation of microbiota were evaluated. The results demonstrated that microbial communities in the jejunum were distinct from those in the cecum, and the microbial community change was more significant in jejunum. Challenge of CP1 in conjunction with Eimeria significantly reduced species diversity in jejunal microbiota, but cecal microbiota remained stable. In the jejunum, CP1 challenge increased the abundance of the genera of Clostridium sensu stricto 1 , Escherichia Shigella , and Weissella , but significantly decreased the population of Lactobacillus . Eimeria infection on its own was unable to promote NE, demonstrating decrements of Clostridium sensu stricto 1 and Lactobacillus . Co-infection with CP1 and Eimeria reproduced the majority of NE lesions with significant increment of C lostridium sensu stricto 1 and reduction in Lactobacillus . The advance of changes on these two taxa increased the severity of NE lesions. Further analyses of metagenomeSeq, STAMP, and LEfSe consistently showed significant overgrowth of Clostridium sensu stricto 1 was associated with NE. The supplementation of lauric acid did not reduce NE incidence and severity but decreased the relative abundance of Escherichia Shigella . In conclusion, significant overgrowth of C . perfringens as well as other Clostridium species in Clostridium sensu stricto 1 with the decrement of Lactobacillus in the jejunum is the featured microbiota correlated with NE. Controlling proliferation of Clostridium sensu stricto 1 and manipulation of Lactobacillus in the jejunum should be the strategy to prevent NE.

A mouse model of chronic liver fibrosis was successfully established by injecting 100 mg kg(-1) TAA three times weekly in male ICR mice. Meanwhile, silymarin showed hepatoprotection against TAA-induced damage.

Nonalcoholic fatty liver (NAFL) is also called hepatic steatosis and has become an emergent liver disease in developed and developing nations. This study was to exam the preventive effects of taurine (Tau) on the development of hepatic steatosis via a hamster model. Although hepatic steatosis of hamsters was induced by feeding a high-fat/cholesterol diet, drinking water containing 0.35 and 0.7% Tau improved (p < 0.05) the serum lipid profile. Meanwhile, the smaller (p < 0.05) liver sizes and lower (p < 0.05) hepatic lipids in high-fat/cholesterol dietary hamsters drinking Tau may be partially due to higher (p < 0.05) fecal cholesterol, triacylglycerol, and bile acid outputs. In the regulation of lipid homeostasis, drinking a Tau solution upregulated (p < 0.05) low-density lipoprotein receptor and CYP7A1 gene expressions in high-fat/cholesterol dietary hamsters, which result in increased fecal cholesterol and bile acid outputs. Drinking a Tau solution also upregulated (p < 0.05) peroxisome proliferator-activated receptor-α (PPAR-α) and uncoupling protein 2 (UPC2) gene expressions in high-fat/cholesterol dietary hamsters, thus increasing energy expenditure. Besides, Tau also enhanced (p < 0.05) liver antioxidant capacities (GSH, TEAC, SOD, and CAT) and decreased (p < 0.05) lipid peroxidation (MDA), which alleviated liver damage in the high-fat/cholesterol dietary hamsters. Therefore, Tau shows preventive effects on the development of hepatic steatosis induced by a high-fat/cholesterol dietary habit.

Rectal swabs were collected from 437 household and 491 stray dogs in northern Taiwan from May 2003 to June 2005 to investigate the prevalence and antimicrobial susceptibilities of salmonellae and campylobacters. The results revealed that 2.1% of household dogs and 6.3% of stray dogs were positive for salmonellae, with Salmonella Duesseldorf being the most dominant serotype in both. Additionally, 2.7% of the household dogs and 23.8% of the stray dogs were positive for campylobacters. Campylobacter jejuni was the most prevalent species (86.8%), followed by C. upsaliensis (9.3%) and C. coli (3.9%). Both salmonella and campylobacter isolation rates from the stray dogs were significantly higher than those from the household dogs (p < 0.01). The susceptibility of 33 C. jejuni isolates to eight antimicrobials was studied by the E-test. A high rate of resistance was observed to azithromycin (93.9%), clindamycin (87.9%), erythromycin (81.8%), tetracycline (78.8%), chloramphenicol (69.7%), nalidixic acid (51.5%), gentamicin (33.3%), and ciprofloxacin (18.2%). The susceptibility of 40 Salmonella isolates to 15 antimicrobials was also studied by the disc-diffusion method. All the Salmonella isolates were susceptible to ciprofloxacin and ceftriaxone. Resistance was observed most frequently to tetracycline (77.5%), chloramphenicol (52.5%), and ampicillin (50%).

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Summary This study was divided into two parts: (i) an optimal hydrolysing procedure of chicken liver hydrolysates (CLHs) and (ii) the in vivo antioxidant properties of CLHs via a D‐galactose‐induced mouse model. A pepsin‐to‐raw chicken liver mass ratio (1:400, w:w) and 2‐h hydrolysing period were chosen to manufacture CLHs based on yield, peptide level and antioxidant effect. Molecular masses of CLHs were lower than 10 kDa. CLH was rich in aspartic acid and glutamic acid, and also contained both manganese and selenium, which are essential cofactors of superoxide dismutase and glutathione peroxidase, respectively. The contents of cadmium, mercury, tin, and arsenic in CLHs were very low and even no detectible. Regarding the in vivo antioxidant activity of CLHs, a dosage of 1.2 g D‐galactose kg−1 body weight increased (P < 0.05) 2‐thiobarbituric acid reactive substances values and decreased (P < 0.05) glutathione and Trolox equivalent antioxidant capacity values, as well as superoxide dismutase, catalase, and glutathione peroxidase activities in serum and organs of mice. However, the in vivo antioxidant capacities were improved (P < 0.05) by supplementing CLHs.

Noni juice (NJ) is rich in phytochemicals and polysaccharides. Lipid-lowering and antioxidative effects of NJ were investigated in this study. Fifty male hamsters were assigned randomly to one of the following groups: (1) normal diet and distilled water (LFCD); (2) high-fat/cholesterol diet and distilled water (HFCD); (3) HFCD and 3 ml NJ (including 0.20 g solids)/kg BW (NJ_L); (4) HFCD and 6 mL NJ (including 0.40 g solids)/kg BW (NJ_M); (5) HFCD and 9 ml NJ (including 0.60 g solids)/kg BW (NJ_H) for six weeks. NJ supplementation decreased (p < 0.05) serum triacylglycerol, cholesterol, atherogenic index, malondialdehyde levels, and hepatic lipids in HFCD hamsters, whereas serum trolox equivalent antioxidant capacity, glutathione, and fecal lipids in HFCD hamsters were increased (p < 0.05) by NJ supplementation. Although NJ supplementation downregulated (p < 0.05) sterol regulator element binding protein-1c in HFCD hamsters, it upregulated (p < 0.05) hepatic peroxisome proliferator-activated receptor-alpha and uncoupling protein 2 gene expressions in HFCD hamsters. Results demonstrate that NJ promotes cardioprotection in a high-fat/cholesterol diet.

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