Selenomethionine Mitigates Effects of Nocardia cyriacigeorgica-Induced Inflammation, Oxidative Stress, and Apoptosis in Bovine Mammary Epithelial Cells

<i>Nocardia cyriacigeorgica</i> causes bovine mastitis, reduces milk quantity and quality, and is often resistant to antimicrobials. Selenomethionine (SeMet) is a form of selenium, which reduces reactive oxygen species (ROS)-mediated apoptosis and intramammary infections. However, the protective effects of SeMet on <i>N. cyriacigeorgica</i>-infected bovine mammary epithelial cells (bMECs) are unclear. The objective of this study was to evaluate whether SeMet mitigated <i>N. cyriacigeorgica</i>-induced inflammatory injury, oxidative damage and apoptosis in bMECs. Cells were cultured with or without being pretreated with 40 µM of SeMet for 12 h, then challenged with <i>N. cyriacigeorgica</i> (multiplicity of infection = 5:1) for 6 h. Although <i>N. cyriacigeorgica</i> was resistant to lincomycin, erythromycin, enrofloxacin, penicillin, amoxicillin, cephalonium, cephalexin, and ceftriaxone, 40 μM SeMet increased cell viability and inhibited lactate dehydrogenase release in infected bMECs. Furthermore, <i>N. cyriacigeorgica</i> significantly induced mRNA production and protein expression of TNF-α, IL-1β, IL-6, and IL-8 at 6 h. Cell membrane rupture, cristae degeneration and mitochondria swelling were evident with transmission electron microscopy. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) activities were down-regulated after 3, 6, or 12 h, whereas malondialdehyde (MDA) and ROS contents were significantly upregulated, with cell damage and apoptosis rapidly evident (the latter increased significantly in a time-dependent manner). In contrast, bMECs pretreated with 40 μM SeMet before infection, SOD, and GSH-px activities were upregulated (<i>p</i> < 0.05); MDA and ROS concentrations were downregulated (<i>p</i> < 0.05), and apoptosis was reduced (<i>p</i> < 0.05). In conclusion, 40 μM SeMet alleviated inflammation, oxidative stress and apoptosis induced by <i>N. cyriacigeorgica</i> in bMECs <i>cultured</i> in vitro.

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Publication Details

Journal
International Journal of Molecular Sciences
Published
2024-10-12
DOI
https://doi.org/10.3390/ijms252010976
Citations
2
Primary Topic
Actinomycetales infections and treatment
Type
article
Field-Weighted Citation Impact
3.15

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article

Selenomethionine Mitigates Effects of Nocardia cyriacigeorgica-Induced Inflammation, Oxidative Stress, and Apoptosis in Bovine Mammary Epithelial Cells

Jinge Han, Herman W. Barkema, John P. Kastelic, Bo Han et al.
2 citations
International Journal of Molecular Sciences
Actinomycetales infections and treatment
3.15
article

Selenomethionine Mitigates Effects of Nocardia cyriacigeorgica-Induced Inflammation, Oxidative Stress, and Apoptosis in Bovine Mammary Epithelial Cells

Jinge Han, Herman W. Barkema, John P. Kastelic, Bo Han, Xueying Zhou, Talgat Assabayev, Halihaxi Bahetijiang, Venera Abdrassilova, Muhammad Asfandyar Khan, Gang Liu
article en
2 citations

Abstract

<i>Nocardia cyriacigeorgica</i> causes bovine mastitis, reduces milk quantity and quality, and is often resistant to antimicrobials. Selenomethionine (SeMet) is a form of selenium, which reduces reactive oxygen species (ROS)-mediated apoptosis and intramammary infections. However, the protective effects of SeMet on <i>N. cyriacigeorgica</i>-infected bovine mammary epithelial cells (bMECs) are unclear. The objective of this study was to evaluate whether SeMet mitigated <i>N. cyriacigeorgica</i>-induced inflammatory injury, oxidative damage and apoptosis in bMECs. Cells were cultured with or without being pretreated with 40 µM of SeMet for 12 h, then challenged with <i>N. cyriacigeorgica</i> (multiplicity of infection = 5:1) for 6 h. Although <i>N. cyriacigeorgica</i> was resistant to lincomycin, erythromycin, enrofloxacin, penicillin, amoxicillin, cephalonium, cephalexin, and ceftriaxone, 40 μM SeMet increased cell viability and inhibited lactate dehydrogenase release in infected bMECs. Furthermore, <i>N. cyriacigeorgica</i> significantly induced mRNA production and protein expression of TNF-α, IL-1β, IL-6, and IL-8 at 6 h. Cell membrane rupture, cristae degeneration and mitochondria swelling were evident with transmission electron microscopy. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) activities were down-regulated after 3, 6, or 12 h, whereas malondialdehyde (MDA) and ROS contents were significantly upregulated, with cell damage and apoptosis rapidly evident (the latter increased significantly in a time-dependent manner). In contrast, bMECs pretreated with 40 μM SeMet before infection, SOD, and GSH-px activities were upregulated (<i>p</i> < 0.05); MDA and ROS concentrations were downregulated (<i>p</i> < 0.05), and apoptosis was reduced (<i>p</i> < 0.05). In conclusion, 40 μM SeMet alleviated inflammation, oxidative stress and apoptosis induced by <i>N. cyriacigeorgica</i> in bMECs <i>cultured</i> in vitro.

International Journal of Molecular SciencesVol. 25(20)
Tianjin Agricultural University (CN), University of Calgary (CA), Kazakh National Medical University (KZ), China Agricultural University (CN)
National Natural Science Foundation of China
Life below water
Openalex Percentile: Top 9%
Actinomycetales infections and treatment
3.15
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