Histological Lesions, Cell Cycle Arrest, Apoptosis and  T Cell Subsets Changes of Spleen in Chicken Fed  Aflatoxin-contaminated Corn

Peng, Xi; Zhang, Keying; Bai, Shiping; Ding, Xuemei; Zeng, Qiufeng; Yang, Jun; Fang, Jing; Chen, Kejie

doi:10.3390/ijerph110808567

Cited by 43 publications

(46 citation statements)

References 35 publications

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“…Similar to the results of previous studies, we found that the weights of the spleens were significantly increased during aflatoxicosis at 2 mg AFB 1 /kg of feed at 21 DPF (Huff et al, 1986;Peng et al, 2014a;Fowler et al, 2015).…”

Section: Discussionsupporting

confidence: 81%

Biochemical and Histopathological Study of Aflatoxicosis on Ross 308 Broiler Chicks

Ko¹,

Ahn²,

Shin³

et al. 2017

Korean J. Poult. Sci.

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Totally, one hundred and sixty 1-day-old Ross 308 broiler chicks were fed with a diet containing 0, 0.5, 1.0, and 2.0 mg of aflatoxin B 1 (AFB 1 )/kg of feed for 21 days. Body weight was lower for the AFB 1 -treated broilers than for the control group. At 14 and 21 DPF, the broilers fed with 2.0 mg of AFB 1 /kg of feed weighed significantly lower than those of the other groups (p<0.05). Relative liver weights increased significantly in a dose-dependent manner, and relative spleen weights were significantly high in the chicks fed with 2.0 mg of AFB 1 /kg of feed at 21 DPF (p<0.001). Biochemical analyses showed that total protein and albumin levels decreased significantly at 7 and 14 DPF for the chicks of the group fed with 2.0 of mg AFB 1 /kg of feed, compared with those fed with 0.5 and 1.0 mg of AFB 1 /kg of feed (p<0.05). AST and ALT levels increased significantly at 14 and 21 DPF (p<0.05), and the AST levels, particularly, increased dose-dependently (p<0.05). Histopathological analyses showed that the liver tissues of the AFB 1 -treated chicks showed significant lesions, including hemorrhage, hepatocyte necrosis, inflammatory cell infiltration, and fatty degeneration. The severity of both hepatocyte necrosis and inflammatory cell infiltration appeared to increase dose-and time-dependently. Similarly, hepatic fibrosis increased dosedependently (p<0.05). The results of this study could improve our understanding of parameters used for evaluating aflatoxicosis in poultry.

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Section: Discussionsupporting

confidence: 81%

Biochemical and Histopathological Study of Aflatoxicosis on Ross 308 Broiler Chicks

Ko¹,

Ahn²,

Shin³

et al. 2017

Korean J. Poult. Sci.

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“…Since avian immune system relies on B cells, T cells and spleen functionality, any destruction in bursa of Fabricius, thymus and spleen could be associated with impaired immunological responses (Girish & Smith, ). Histopathological observation of the spleen showed that elevated relative weight of spleen caused by aflatoxins could be due to the congestion of red pulp in the spleen (Peng et al, ). Reversing the negative effects of AFB 1 on immune organs by Ex‐TRP diet may be governed either by kynurenine production or by antioxidant properties of TRP derivatives such as 5‐hydroxytryptophan and melatonin, resulting in the healing of congestion of red pulp in the spleen.…”

Section: Discussionmentioning

confidence: 99%

Excess dietary tryptophan mitigates aflatoxicosis in growing quails

khanipour

Mehri

Kasmani

et al. 2019

Animal Physiology Nutrition

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A biological assay was carried out to evaluate the impact of dietary tryptophan (TRP) in aflatoxin B1‐contaminated diets (AFB1‐D) on performance, blood parameters, immunity, meat quality and microbial populations of intestine in Japanese quails. Six experimental diets were formulated to include two levels of dietary TRP; 2.9 (moderate high: MH‐TRP) and 4.9 g/kg (excess: Ex‐TRP); and three levels of AFB1 (0.0, 2.5, and 5.0 mg/kg). Each experimental diet was fed to the one of the six groups of birds from 7 to 35 days of age in a completely randomized design with 2 × 3 factorial arrangement. Decrease in feed intake, body weight gain and gain:feed in birds fed 5.0 mg/kg AFB1‐D was restored to the control level by 4.9 g TRP/kg of the diet. The hepatic enzymes in blood were elevated in quails fed on AFB1‐D but attenuated by 4.9 g TRP/kg of the diet (Ex‐TRP; p ≤ .01). High serum uric acid in birds challenged with AFB1 significantly decreased by Ex‐TRP (p ≤ .01). The skin thickness to 2,4‐dinitro‐1‐chlorobenzene challenge suppressed by AFB1 but increased by Ex‐TRP diet (p ≤ .02). The AFB1 increased the malondialdehyde in meat, whereas TRP efficiently diminished malondialdehyde production (p ≤ .01). The greatest drip loss and pH in meat were observed in the birds fed 5.0 mg/kg AFB1‐D but Ex‐TRP augmented the adverse effects of AFB1 (p ≤ .01). The Ex‐TRP reduced the total microbial and Escherichia coli counts (p ≤ .01). The adverse effect of AFB1 on ileal Lactic acid bacteria was completely prevented by Ex‐TRP (p ≤ .03). This study showed that tryptophan supplementation could be considered as a powerful nutritional tool to ameliorate the adverse effects of AFB1 in growing quails.

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“…AFB1 consumption during growth can lead to immune tissue atrophy, reducing relative weights of the bursa, spleen and thymus [120,122,134,139,[149][150][151][152]. Increases in relative spleen weight have also been observed during aflatoxicosis [117,120,[153][154][155][156]. In young chickens, tissue changes are concomitant to the development of histopathological lesions.…”

Section: Immunotoxicitymentioning

confidence: 99%

“…In young chickens, tissue changes are concomitant to the development of histopathological lesions. AFB1 exposure causes visible congestion in the spleen and thymus, while nuclear debris accumulates in the thymus and bursa [139,149,150,156]. In AFB1-exposed chicks, vacuoles increase in the lymphoid follicles of the bursa and the white pulp of the spleen, especially the T-cell rich periarteriolar lymphoid sheaths [139,150,156].…”

Section: Immunotoxicitymentioning

confidence: 99%

“…This likely results from increased apoptosis of splenocytes, thymocytes and bursal B-cells as seen in young chickens during aflatoxicosis [139,149,156,169,170]. In the chicken, both CD4 + and CD8 + T lymphocytes in the spleen, thymus, peripheral blood, and even the ileum can be affected by AFB1 exposure [149,150,156,168,171,172]. Oxidative stress and DNA damage from AFB1 are likely responsible for initiating apoptotic processes in lymphocytes [169,170].…”

Section: Immunotoxicitymentioning

confidence: 99%

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Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

2015

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This review is a comprehensive introduction to the effects of poultry exposure to the toxic and carcinogenic mycotoxin aflatoxin B1 (AFB1). The relationship between AFB1 sensitivity and metabolism, major direct and indirect effects of AFB1, recent studies of gene expression and transcriptome responses to exposure, and mitigation strategies to reduce toxicity are discussed. Exposure to AFB1 primarily occurs by consumption of contaminated corn, grain or other feed components. Low levels of residual AFB1 in poultry feeds can cause reduction in growth, feed conversion, egg production, and compromised immune functions, resulting in significant economic costs to producers. Thus, AFB1 acts as a "force multiplier" synergizing the adverse effects of microbial pathogens and other agents, and factors detrimental to poultry health. Domestic turkeys (Meleagris gallopavo) are one of the most sensitive animals known to AFB1 due, in large part, to a combination of efficient hepatic bioactivation by cytochromes P450 1A5 and 3A37, and deficient hepatic glutathione-S-transferase (GST)-mediated detoxification. Because of their sensitivity, turkeys are a good model to investigate chemopreventive treatments and feed additives for their ability to reduce AFB1 toxicity. Transcriptome analysis (RNA-seq) of turkey poults (liver and spleen) has identified AFB1-induced gene expression changes in pathways of apoptosis, carcinogenesis, lipid regulation, antimicrobial activity, cytotoxicity and antigen presentation. Current research focuses on further identifying the molecular mechanisms OPEN ACCESSAgriculture 2015, 5 743 underlying AFB1 toxicity with the goal of reducing aflatoxicosis and improving poultry health.

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Histological Lesions, Cell Cycle Arrest, Apoptosis and T Cell Subsets Changes of Spleen in Chicken Fed Aflatoxin-contaminated Corn

Cited by 43 publications

References 35 publications

Biochemical and Histopathological Study of Aflatoxicosis on Ross 308 Broiler Chicks

Biochemical and Histopathological Study of Aflatoxicosis on Ross 308 Broiler Chicks

Excess dietary tryptophan mitigates aflatoxicosis in growing quails

Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

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