Protective effects of Lactobacillus on heat stress-induced intestinal injury in finisher broilers by regulating gut microbiota and stimulating epithelial development.

Heat stress (HS) is a critical challenge in broilers due to the high metabolic rate and lack of sweat glands. Results from this study show that implementing a cyclic chronic HS (34 °C for 7 h/d) to finisher broilers decreased the diversity of cecal microbiota and impaired intestinal barrier, resulting in gut leak and decreased body weight (both P < 0.05). These alterations might be related to inflammatory outbursts and the retarded proliferation of intestinal epithelial cells (IECs) according to the transcriptome analysis. Considering the potential beneficial properties of Lactobacillus on intestinal development and function, the protective effects of Lactobacillus rhamnosus (L. rhamnosus) on the intestine were investigated under HS conditions in this study. Orally supplemented L. rhamnosus improved the composition of cecal microbiota and upregulated the transcription of tight junction proteins in both duodenum and jejunum, with a consequent suppression in intestinal gene expressions of pro-inflammatory cytokines and facilitation in digestive capability. Meanwhile, the jejunal villus height of the birds that received L. rhamnosus was significantly higher compared with those treated with the broth (P < 0.05). The expression abundances of genes related to IECs proliferation and differentiation were increased by L. rhamnosus, along with upregulated mRNA levels of Wnt3a and ß-catenin in jejunum. In addition, L. rhamnosus attenuated enterocyte apoptosis as indicated by decreased caspase-3 and caspase-9 gene expressions. The results indicated that oral administration with L. rhamnosus mitigated HS-induced dysfunction by promoting intestinal development and epithelial maturation in broilers and that the effects of L. rhamnosus might be dependent of Wnt/ß-catenin signaling.

The kinetics of glutathione in the gastrointestinal tract of weaned piglets supplemented with different doses of dietary reduced glutathione.

This study aimed to investigate the kinetics of dietary GSH in the gastrointestinal tract and the effect of GSH on the intestinal redox status of weaned piglets. Forty-eight piglets with an average age of 26 days and an average body weight of 7.7 kg were used in this study. The piglets were divided into three treatment groups including the control group with a basal diet (CON) and two GSH groups with a basal diet supplemented with 0.1% GSH (LGSH) and 1.0% GSH (HGSH), respectively. The basal diet did not contain any GSH. The experiment lasted for 14 days, with eight animals sampled from each group on d5 and 14. The parts of 0-5%, 5-75%, and 75-100% of the length of the small intestine were assigned to SI1, SI2, and SI3. The results showed that GSH almost completely disappeared from the digesta at SI2. However, no difference in the GSH level in mucosa, liver, and blood erythrocytes was found. The level of cysteine (CYS) in SI1 digesta was significantly higher in HGSH than CON and LGSH on d14, and similar findings were observed for cystine (CYSS) in SI3 digesta on d5. The CYSS level in HGSH was also significantly higher than LGSH in the stomach on d14, while no CYS or CYSS was detected in the stomach for control animals, indicating the breakdown of GSH to CYS already occurred in the stomach. Irrespective of the dietary treatment, the CYS level on d14 and the CYSS level on d5 and 14 were increased when moving more distally into the gastrointestinal tract. Furthermore, the mucosal CYS level was significantly increased at SI1 in the LGSH and HGSH group compared with CON on d5. Glutathione disulfide (GSSG) was recovered in the diets and digesta from the LGSH and HGSH group, which could demonstrate the auto-oxidation of GSH. It is, therefore, concluded that GSH supplementation could not increase the small intestinal mucosal GSH level of weaned piglets, and this could potentially relate to the kinetics of GSH in the digestive tract, where GSH seemed to be prone to the breakdown to CYS and CYSS and the auto-oxidation to GSSG.

Interplay between zinc and cell proliferation and implications for the growth of livestock.

Zinc (Zn) plays a critical role in the growth of livestock, which depends on cell proliferation. In addition to modifying the growth associated with its effects on food intake, mitogenic hormones, signal transduction and gene transcription, Zn also regulates body weight gain through mediating cell proliferation. Zn deficiency in animals leads to growth inhibition, along with an arrest of cell cycle progression at G0/G1 and S phase due to depression in the expression of cyclin D/E and DNA synthesis. Therefore, in the present study, the interplay between Zn and cell proliferation and implications for the growth of livestock were reviewed, in which Zn regulates cell proliferation in several ways, especially cell cycle progression at the G0/G1 phase DNA synthesis and mitosis. During the cell cycle, the Zn transporters and major Zn binding proteins such as metallothioneins are altered with the requirements of cellular Zn level and nuclear translocation of Zn. In addition, calcium signaling, MAPK pathway and PI3K/Akt cascades are also involved in the process of Zn-interfering cell proliferation. The evidence collected over the last decade highlights the necessity of Zn for normal cell proliferation, which suggests Zn supplementation should be considered for the growth and health of poultry.

The Blood Immune Cell Count, Immunoglobulin, Inflammatory Factor, and Milk Trace Element in Transition Cows and Calves Were Altered by Increasing the Dietary n-3 or n-6 Polyunsaturated Fatty Acid Levels.

Transition dairy cows experience sudden changes in both metabolic and immune functions, which lead to many diseases in postpartum cows. Therefore, it is crucial to monitor and guarantee the nutritional and healthy status of transition cows. The objective of this study was to determine the effect of diet enriched in n-3 or n-6 polyunsaturated fatty acid (PUFA) on colostrum composition and blood immune index of multiparous Holstein cows and neonatal calves during the transition period. Forty-five multiparous Holstein dairy cows at 240 days of pregnancy were randomly assigned to receive 1 of 3 isoenergetic and isoprotein diets: 1) CON, hydrogenated fatty acid (control), 1% of hydrogenated fatty acid [diet dry matter (DM) basis] during prepartum and postpartum, respectively; 2) HN3, 3.5% of extruding flaxseed (diet DM basis, n-3 PUFA source); 3) HN6, 8% of extruding soybeans (diet DM basis, C18:2n-6 PUFA source). Diets containing n-3 and n-6 PUFA sources decreased colostrum immunoglobulin G (IgG) concentration but did not significantly change the colostrum IgG yield compared with those with CON. The commercial milk yield (from 14 to 28 days after calving) was higher in the HN3 and HN6 than that in the CON. Furthermore, the n-3 PUFA source increased neutrophil cell counts in blood during the prepartum period and increased neutrophil percentage during the postpartum period when compared with those with control treatment. Diets containing supplemental n-3 PUFA decreased the serum concentration of interleukin (IL)-1ß in maternal cows compared with those in control and n-6 PUFA during prepartum and postpartum. In addition, the neonatal calf serum concentration of tumor necrosis factor (TNF) was decreased in HN3 compared with that in the HN6 treatment. The diet with the n-3 PUFA source could potentially increase the capacity of neutrophils to defend against pathogens in maternal cows by increasing the neutrophil numbers and percentage during the transition period. Meanwhile, the diet with n-3 PUFA source could decrease the pro-inflammatary cytokine IL-1ß of maternal cows during the transition period and decline the content of pro-inflammatary cytokine TNF of neonatal calves. It suggested that the highest milk production in n-3 PUFA treatment may partially be due to these beneficial alterations.