Aflatoxicosis chemoprevention by probiotic Lactobacillius and lack of effect on the major histocompatibility complex

Sumit Rawal; Miranda M. Bauer; Kristelle M. Mendoza; Hani El-Nezami; Jeffery R. Hall; Ji Eun Kim; John R. Stevens; Kent M. Reed; Roger A. Coulombe

doi:10.1016/j.rvsc.2014.06.008

Aflatoxicosis chemoprevention by probiotic Lactobacillius and lack of effect on the major histocompatibility complex

Sumit Rawal, Miranda M. Bauer, Kristelle M. Mendoza, Hani El-Nezami, Jeffery R. Hall, Ji Eun Kim, John R. Stevens, Kent M. Reed, Roger A. Coulombe

Veterinary and Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

Turkeys are extremely sensitive to aflatoxin B₁ (AFB₁) which causes decreased growth, immunosuppression and liver necrosis. The purpose of this study was to determine whether probiotic Lactobacillus, shown to be protective in animal and clinical studies, would likewise confer protection in turkeys, which were treated for 11 days with either AFB₁ (AFB; 1 ppm in diet), probiotic (PB; 1 × 10¹¹ CFU/ml; oral, daily), probiotic + AFB₁ (PBAFB), or PBS control (CNTL). The AFB₁ induced drop in body and liver weights were restored to normal in CNTL and PBAFB groups. Hepatotoxicity markers were not significantly reduced by probiotic treatment. Major histocompatibility complex (MHC) genes BG1 and BG4, which are differentially expressed in liver and spleens, were not significantly affected by treatments. These data indicate modest protection, but the relatively high dietary AFB₁ treatment, and the extreme sensitivity of this species may reveal limits of probiotic-based protection strategies.

Original language	English (US)
Pages (from-to)	274-281
Number of pages	8
Journal	Research in veterinary science
Volume	97
Issue number	2
DOIs	https://doi.org/10.1016/j.rvsc.2014.06.008
State	Published - 2014

Bibliographical note

Funding Information:
The authors thank Moroni Feed Co (Ephraim, UT) for supplying turkeys and feed. This study was funded by USDA-AFRI Grants 2005-01326 , 2007-35205-17880 and 2009-35205-05302 , 2013-01043 from the USDA NIFA Animal Genome Program . Support from the Utah and Minnesota Agricultural Experiments Stations is also gratefully acknowledged. None of these sponsors were involved in this study.

Publisher Copyright:
© 2014 Elsevier Ltd.

Keywords

Aflatoxin
BG
Chemoprevention
Gene expression
MHC
Poultry
Probiotics
Toxicology
Turkeys

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "Aflatoxicosis chemoprevention by probiotic Lactobacillius and lack of effect on the major histocompatibility complex",

abstract = "Turkeys are extremely sensitive to aflatoxin B1 (AFB1) which causes decreased growth, immunosuppression and liver necrosis. The purpose of this study was to determine whether probiotic Lactobacillus, shown to be protective in animal and clinical studies, would likewise confer protection in turkeys, which were treated for 11 days with either AFB1 (AFB; 1 ppm in diet), probiotic (PB; 1 × 1011 CFU/ml; oral, daily), probiotic + AFB1 (PBAFB), or PBS control (CNTL). The AFB1 induced drop in body and liver weights were restored to normal in CNTL and PBAFB groups. Hepatotoxicity markers were not significantly reduced by probiotic treatment. Major histocompatibility complex (MHC) genes BG1 and BG4, which are differentially expressed in liver and spleens, were not significantly affected by treatments. These data indicate modest protection, but the relatively high dietary AFB1 treatment, and the extreme sensitivity of this species may reveal limits of probiotic-based protection strategies.",

keywords = "Aflatoxin, BG, Chemoprevention, Gene expression, MHC, Poultry, Probiotics, Toxicology, Turkeys",

author = "Sumit Rawal and Bauer, {Miranda M.} and Mendoza, {Kristelle M.} and Hani El-Nezami and Hall, {Jeffery R.} and Kim, {Ji Eun} and Stevens, {John R.} and Reed, {Kent M.} and Coulombe, {Roger A.}",

note = "Funding Information: The authors thank Moroni Feed Co (Ephraim, UT) for supplying turkeys and feed. This study was funded by USDA-AFRI Grants 2005-01326 , 2007-35205-17880 and 2009-35205-05302 , 2013-01043 from the USDA NIFA Animal Genome Program . Support from the Utah and Minnesota Agricultural Experiments Stations is also gratefully acknowledged. None of these sponsors were involved in this study. Publisher Copyright: {\textcopyright} 2014 Elsevier Ltd.",

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AU - Mendoza, Kristelle M.

AU - El-Nezami, Hani

AU - Hall, Jeffery R.

AU - Kim, Ji Eun

AU - Stevens, John R.

AU - Reed, Kent M.

AU - Coulombe, Roger A.

N1 - Funding Information: The authors thank Moroni Feed Co (Ephraim, UT) for supplying turkeys and feed. This study was funded by USDA-AFRI Grants 2005-01326 , 2007-35205-17880 and 2009-35205-05302 , 2013-01043 from the USDA NIFA Animal Genome Program . Support from the Utah and Minnesota Agricultural Experiments Stations is also gratefully acknowledged. None of these sponsors were involved in this study. Publisher Copyright: © 2014 Elsevier Ltd.

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N2 - Turkeys are extremely sensitive to aflatoxin B1 (AFB1) which causes decreased growth, immunosuppression and liver necrosis. The purpose of this study was to determine whether probiotic Lactobacillus, shown to be protective in animal and clinical studies, would likewise confer protection in turkeys, which were treated for 11 days with either AFB1 (AFB; 1 ppm in diet), probiotic (PB; 1 × 1011 CFU/ml; oral, daily), probiotic + AFB1 (PBAFB), or PBS control (CNTL). The AFB1 induced drop in body and liver weights were restored to normal in CNTL and PBAFB groups. Hepatotoxicity markers were not significantly reduced by probiotic treatment. Major histocompatibility complex (MHC) genes BG1 and BG4, which are differentially expressed in liver and spleens, were not significantly affected by treatments. These data indicate modest protection, but the relatively high dietary AFB1 treatment, and the extreme sensitivity of this species may reveal limits of probiotic-based protection strategies.

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Aflatoxicosis chemoprevention by probiotic Lactobacillius and lack of effect on the major histocompatibility complex

Abstract

Bibliographical note

Keywords

UN SDGs

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