Heat Stress Causes Immune Abnormalities via Massive Damage to Effect Proliferation and Differentiation of Lymphocytes in Broiler Chickens

The present study evaluated the effect of three feeding methods (dry feed, wet feed or wet feed fermented with Bacillus licheniformis) on the growth performance, intestinal histomorphometry and gene expression of the lipid metabolism- and growth-related genes of broiler chickens. A total of 360 one-day-old Cobb-500 broiler chicks were randomly allotted into three groups containing four replicates with 30 birds each. The first group (control) was fed a dry mash basal diet. The second and third groups were fed wet feed and fermented wet feed. The final body weight and weight gain were reduced (p < 0.01) in the wet feed group, while they did not differ between the fermented wet feed and dry feed groups. Feed intake was not altered, and feeding on wet feed significantly (p < 0.01) increased the feed-to-gain ratio compared to the remaining groups. No differences between the three feeding methods in carcass characteristics, blood biochemistry and nutrient digestibility were observed except for crude protein digestibility, which was increased (p < 0.01) in the fermented wet feed group. Duodenal and ileal villi heights were elevated in birds fed fermented wet feeds, while crypt depth was not altered. The expression fold of IGF-1, GH and m-TOR genes in the pectoral muscle of birds fed wet feed was decreased (p < 0.05), while myostatin gene expression was elevated. Feeding on wet feed reduced the hepatic gene expression of PPARγ and increased that of FAS. In conclusion, wet feed negatively affected the broiler chickens’ efficiency under heat stress; however, fermenting the wet feed with Bacillus licheniformis improved feed utilization and birds’ performance compared to the dry feed group.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Feeding Wet Feed or Wet Feed Fermented by Bacillus licheniformis on Growth Performance, Histopathology and Growth and Lipid Metabolism Marker Genes in Broiler Chickens

Saleh

Shukry

Farrag

et al. 2021

“…Heat stress has a profound deleterious impact on broiler health and well-being. It suppresses immunity and disrupts physiological homeostasis, leading to hypersensitivity to neuroinflammation and metabolic disorders; consequently, production performance is impaired and diminished body weight, body weight gain, and increased feed conversion ratios are noted [50]. These alterations have a harmful effect on neurons and their function, causing brain ultrastructural damage and dysfunction, including mental and emotional disorders expressed at both memory and fear responsive levels [51,52].…”

Section: Discussionmentioning

confidence: 99%

Effect of a Synbiotic Supplement on Fear Response and Memory Assessment of Broiler Chickens Subjected to Heat Stress

Mohammed

Mahmoud

Murugesan³

et al. 2021

The aim of this study was to evaluate the effect of a synbiotic containing a probiotic (Enterococcus faecium, Pediococcus acidilactici, Bifidobacterium animalis, and Lactobacillus reuteri) and a prebiotic (fructooligosaccharides) on fear response, memory assessment, and selected stress indicators in broilers subjected to heat stress. A total of 360 1-day-old Ross 708 chicks were evenly divided among three treatments: a basal diet mixed with a synbiotic at 0 (G-C), 0.5 (G-0.5X), and 1.0 (G-1.0X) g/kg. After 15 d, the broilers were exposed to 32 °C for 9 h daily until 42 d. The object memory test was conducted at 15 day; touch, novel object, and isolation tests were conducted at 35 day; tonic immobility (TI) took place at 41 day. At 42 day, plasma corticosterone and tryptophan concentrations and heterophile/lymphocyte (H/L) ratios were measured. Compared to controls, synbiotic-fed broilers, regardless of concentration, had a shorter latency to make the first vocalization, with higher vocalization rates during the isolation test (p = 0.001). the G-1.0 group had the lowest H/L ratio (p = 0.001), but higher plasma tryptophan concentrations and a greater number of birds could reach the observer during the touch test (p = 0.001 and 0.043, respectively). The current results indicate that the synbiotic can be used as a growth promoter to reduce the fear response and stress state of heat-stressed broilers.

“…In poultry, growing research has specifically demonstrated the negative effects of high ambient temperatures on the immune response. Heat stress also induces several immune defects in the broiler by affecting the maturation of T and B cells in lymphoid tissue [ 30 ].…”

Section: Heat Stressmentioning

confidence: 99%

Modulation of Heat-Shock Proteins Mediates Chicken Cell Survival against Thermal Stress

Shehata

Saadeldin

Tukur

et al. 2020

Heat stress is one of the most challenging environmental stresses affecting domestic animal production, particularly commercial poultry, subsequently causing severe yearly economic losses. Heat stress, a major source of oxidative stress, stimulates mitochondrial oxidative stress and cell dysfunction, leading to cell damage and apoptosis. Cell survival under stress conditions needs urgent response mechanisms and the consequent effective reinitiation of cell functions following stress mitigation. Exposure of cells to heat-stress conditions induces molecules that are ready for mediating cell death and survival signals, and for supporting the cell’s tolerance and/or recovery from damage. Heat-shock proteins (HSPs) confer cell protection against heat stress via different mechanisms, including developing thermotolerance, modulating apoptotic and antiapoptotic signaling pathways, and regulating cellular redox conditions. These functions mainly depend on the capacity of HSPs to work as molecular chaperones and to inhibit the aggregation of non-native and misfolded proteins. This review sheds light on the key factors in heat-shock responses for protection against cell damage induced by heat stress in chicken.