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The intestinal microbiome has been shown to influence animal nutrient metabolism and immune homeostasis. The present study aimed to examine the effect of heat stress on the intestinal microbiome of broilers using pyrosequencing technologies. Ninety-six Arbor Acres broiler chicks were allocated to thermoneutral control (TC; 21 ± 1°C) and high ambient temperature (HT; 31 ± 1°C) groups (6 cages of 8 birds per group), respectively, and raised in 2 controlled climate chambers from 28 to 42 d old. Genomic DNA was extracted from ileal contents isolated from 6 male broiler chicks of each group at 42 d old, and then amplified based on the V3-4 hyper-variable region of 16S rRNA. High temperature had no significant effects, but tended to influence the relative abundance of major phyla and orders in the broilers' ileal microbiota. Analysis of linear effect size feature selection identified 9 discriminative features (genus level, linear discriminant analysis score > 3). Clostridium XIVb, Streptophyta, Faecalibacterium, Rothia, Alistipes, Azospirillum, and Oscillibacter were enriched, while Coprococcus and Streptococcus were reduced in heat-stressed broilers. High temperature significantly influenced the alpha diversity, with higher observed species (P = 0.004), whole-tree phylogenetic diversity (P = 0.002), and Chao 1 (P = 0.002), but the Pielou, Shannon, and Simpson indices were unaltered (P > 0.05), indicating that high temperature increased the ileal microbiota species richness. Based on unweighted UniFrac distance metric matrices, principal component analysis showed that the HT group formed a distinct cluster clearly set apart from the TC group. Analysis of similarity also indicated that samples within groups were more similar to each other than to any samples from other groups (R = 0.626; P = 0.004). In conclusion, high temperature influenced the bacterial composition and community structure of the ileal microbiota of broilers, specifically by increasing the species richness. [ABSTRACT FROM AUTHOR]

In order to measure the real-time variations in body temperature with increasing ambient temperature (AT) at different relative humidity (RH) levels, 60 Jinghong laying hens (35-wk-old) were raised in 3 controlled climate chambers (10 cages with 2 birds per chamber). The RH was fixed at one of 3 levels comprising 35, 50, or 85%, and the AT was increased gradually by 1 degree per 0.5 h from 18 to 35°C in the 3 chambers. The core temperature (CT) and surface temperature (ST) of the hens, as well as the AT in the 3 chambers were recorded at 3 min intervals using mini temperature data loggers. The data were analyzed with a broken-line model to determine the inflection point temperature (IPT, the certain AT above which the body temperature of the hens started to change). The experiment was repeated 3 times on 3 d. The IPTs of the laying hens were 23.89 and 25.46°C based on ST and CT at 50% RH, respectively, which indicated that the upper critical temperature of the thermoneutral zone of hens may be a specific temperature between 23.89°C and 25.46°C. The IPTs of the laying hens were 24.11 and 25.20°C based on ST and CT at RH 35%, respectively, and 21.93 and 24.45°C at RH 85%. The RH significantly affected the IPT of ST (P < 0.001). The IPTs were higher at 35 and 50% RH than that at 85% RH (P < 0.05). The coefficients of variation for the IPTs between individual hens were 2.96 to 4.51, and coefficients of variation for the IPTs for the same bird measured on 3 d were 0.69 to 1.59, thereby indicating that this method for estimating the IPTs of hens is stable and repeatable, although more samples are needed. In conclusion, our results indicate that analyzing the real-time variation in body temperature with increasing AT is a reliable method for estimating the IPT to provide an important reference for regulating the temperature in poultry houses. [ABSTRACT FROM AUTHOR]

In the present study, we investigated the effects of acute heat stress on the concentration of free Ca2+ ([Ca2+]i) and markers of cellular immunity in splenic lymphocytes from broiler chickens. Eighty 6-wk-old male broilers were randomly allocated to 2 treatments and exposed to 25 and 35°C (RH, 50 ± 5%) for 3 h. We observed that 3 h of heat exposure (35 ± 1°C, 50 ± 5% RH) increased the body temperature and respiratory rate of broiler chickens significantly, but plasma levels of corticosterone were not changed. Examination of [Ca2+]i and the proliferation of splenic lymphocytes isolated from heat-stressed broiler chickens, using fura-2-acetoxymethyl ester and Cell Counting Kit-8, respectively, showed that acute heat stress caused a significant increase in [Ca2+]i and enhanced concaAavalin A-stimulated but not lipopolysaccharidestimulated lymphocyte proliferation significantly. Flow cytometric analysis of the cell cycle and T-lymphocyte subsets (CD4+ and CD8+) indicated that heat stress promoted the transition of lymphocytes from gap phase 1 to synthesis phase and increased the ratio of CD4+ to CD18+ of T lymphocytes. In addition, acute heat stress enhanced the secretion of interleukin-2 by splenic lymphbcytes significantly. These results suggest that the effect of acute heat stress to increase the [Ca2+]i in lymphocytes may be an early event that enhances Con A-stimulated T-cell proliferation and interleukin-2 secretion and promotes the transition of T cells from gap phase 1 to synthesis phase. [ABSTRACT FROM AUTHOR]

This study investigated the effects of different acute high ambient temperatures on dysfunction of hepatic mitochondrial respiration, the antioxidative enzyme system, and oxidative injury in broiler chickens. One hundred twenty-eight 6-wk-old broiler chickens were assigned randomly to 4 groups and subsequently exposed to 25 (control), 32, 35, and 38°C (RH, 70 ± 5%) for 3 h, respectively. The rectal temperatures, activity of antioxidative enzymes (superoxide dismutase, catalase, and glutathione peroxidase), content of malondialdehyde and protein carbonyl, and the activity of mitochondrial respiratory enzymes were determined. The results showed that exposure to high ambient temperature induced a significant elevation of rectal temperature, antioxidative enzyme activity, and formation of malondialdehyde and protein carbonyl, as well as dysfunction of the mitochondrial respiratory chain in comparison with control (P < 0.05). Almost all of the indicators changed in a temperature-dependent manner with the gradual increase of ambient temperature from 32 to 38°C; differences in each parameter (except catalase) among the groups exposed to different high ambient temperatures were also statistically significant (P < 0.05). The results of the present study suggest that, in the broiler chicken model used here, acute exposure to high temperatures may depress the activity of the mitochondrial respiratory chain. This inactivation results subsequently in overproduction of reactive oxygen species, which ultimately results in oxidative injury. However, this hypothesis needs to be evaluated more rigorously in future studies. It has also been shown that, with the gradual increase in temperature, the oxidative injury induced by heat stress in broiler chickens becomes increasingly severe, and this stress response presents in a temperature-dependent manner in the temperature range of 32 to 38°C. [ABSTRACT FROM AUTHOR]