Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling
Mycobacterium bovis is the causative agent of bovine tuberculosis, has been identified a serious threat to human population. It has been found that sodium butyrate (NaB), the inhibitor of histone deacetylase, can promote the expression of cathelicidin (LL37) and help the body to resist a variety of...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2020-03-01
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| Series: | Frontiers in Microbiology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fmicb.2020.00433/full |
| _version_ | 1829100650412113920 |
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| author | Kai Zhang Tariq Hussain Tariq Hussain Jie Wang Mengying Li Wenjia Wang Xiaojing Ma Yi Liao Jiao Yao Yinjuan Song Zhengmin Liang Xiangmei Zhou Lihua Xu |
| author_facet | Kai Zhang Tariq Hussain Tariq Hussain Jie Wang Mengying Li Wenjia Wang Xiaojing Ma Yi Liao Jiao Yao Yinjuan Song Zhengmin Liang Xiangmei Zhou Lihua Xu |
| author_sort | Kai Zhang |
| collection | DOAJ |
| description | Mycobacterium bovis is the causative agent of bovine tuberculosis, has been identified a serious threat to human population. It has been found that sodium butyrate (NaB), the inhibitor of histone deacetylase, can promote the expression of cathelicidin (LL37) and help the body to resist a variety of injuries. In the current study, we investigate the therapeutic effect of NaB on the regulation of host defense mechanism against M. bovis infection. We found an increased expression of LL37 in M. bovis infected THP-1 cells after NaB treatment. In contrast, NaB treatment significantly down-regulated the expression of Class I HDAC in THP-1 cells infected with M. bovis. Additionally, NaB reduced the expression of phosphorylated P65 (p-P65) and p-IκBα, indicating the inhibition of nuclear factor-κB (NF-κB) signaling. Furthermore, we found that NaB treatment reduced the production of inflammatory cytokines (IL-1β, TNF-α, and IL-10) and a key anti-apoptotic marker protein Bcl-2 in THP-1 cell infected with M. bovis. Notably, mice showed high resistance to M. bovis infection after NaB treatment. The reduction of viable M. bovis bacilli indicates that NaB-induced inhibition of M. bovis infection mediated by upregulation of LL37 and inhibition of NF-κB signaling pathway. These observations illustrate that NaB mediate protective immune responses against M. bovis infection. Overall, these results suggest that NaB can be exploited as a therapeutic strategy for the control of M. bovis in animals and human beings. |
| first_indexed | 2024-12-10T22:35:26Z |
| format | Article |
| id | doaj.art-a2da82f18697471a9d6eef97665e6919 |
| institution | Directory Open Access Journal |
| issn | 1664-302X |
| language | English |
| last_indexed | 2024-12-10T22:35:26Z |
| publishDate | 2020-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Microbiology |
| spelling | doaj.art-a2da82f18697471a9d6eef97665e69192022-12-22T01:30:54ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2020-03-011110.3389/fmicb.2020.00433501039Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB SignalingKai Zhang0Tariq Hussain1Tariq Hussain2Jie Wang3Mengying Li4Wenjia Wang5Xiaojing Ma6Yi Liao7Jiao Yao8Yinjuan Song9Zhengmin Liang10Xiangmei Zhou11Lihua Xu12School of Agriculture, Ningxia University, Yinchuan, ChinaKey Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, ChinaCollege of Veterinary Sciences, The University of Agriculture Peshawar, Peshawar, PakistanInstitute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Comparative Medicine Center, Peking Union Medical College, Beijing, ChinaSchool of Agriculture, Ningxia University, Yinchuan, ChinaSchool of Agriculture, Ningxia University, Yinchuan, ChinaSchool of Agriculture, Ningxia University, Yinchuan, ChinaKey Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, ChinaKey Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, ChinaKey Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, ChinaKey Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, ChinaKey Laboratory of Animal Epidemiology and Zoonosis, Ministry of Agriculture, National Animal Transmissible Spongiform Encephalopathy Laboratory, College of Veterinary Medicine, China Agricultural University, Beijing, ChinaSchool of Agriculture, Ningxia University, Yinchuan, ChinaMycobacterium bovis is the causative agent of bovine tuberculosis, has been identified a serious threat to human population. It has been found that sodium butyrate (NaB), the inhibitor of histone deacetylase, can promote the expression of cathelicidin (LL37) and help the body to resist a variety of injuries. In the current study, we investigate the therapeutic effect of NaB on the regulation of host defense mechanism against M. bovis infection. We found an increased expression of LL37 in M. bovis infected THP-1 cells after NaB treatment. In contrast, NaB treatment significantly down-regulated the expression of Class I HDAC in THP-1 cells infected with M. bovis. Additionally, NaB reduced the expression of phosphorylated P65 (p-P65) and p-IκBα, indicating the inhibition of nuclear factor-κB (NF-κB) signaling. Furthermore, we found that NaB treatment reduced the production of inflammatory cytokines (IL-1β, TNF-α, and IL-10) and a key anti-apoptotic marker protein Bcl-2 in THP-1 cell infected with M. bovis. Notably, mice showed high resistance to M. bovis infection after NaB treatment. The reduction of viable M. bovis bacilli indicates that NaB-induced inhibition of M. bovis infection mediated by upregulation of LL37 and inhibition of NF-κB signaling pathway. These observations illustrate that NaB mediate protective immune responses against M. bovis infection. Overall, these results suggest that NaB can be exploited as a therapeutic strategy for the control of M. bovis in animals and human beings.https://www.frontiersin.org/article/10.3389/fmicb.2020.00433/fullMycobacterium bovissodium butyratehistone deacetylationNuclear factor-κBcathelicidin |
| spellingShingle | Kai Zhang Tariq Hussain Tariq Hussain Jie Wang Mengying Li Wenjia Wang Xiaojing Ma Yi Liao Jiao Yao Yinjuan Song Zhengmin Liang Xiangmei Zhou Lihua Xu Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling Frontiers in Microbiology Mycobacterium bovis sodium butyrate histone deacetylation Nuclear factor-κB cathelicidin |
| title | Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling |
| title_full | Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling |
| title_fullStr | Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling |
| title_full_unstemmed | Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling |
| title_short | Sodium Butyrate Abrogates the Growth and Pathogenesis of Mycobacterium bovis via Regulation of Cathelicidin (LL37) Expression and NF-κB Signaling |
| title_sort | sodium butyrate abrogates the growth and pathogenesis of mycobacterium bovis via regulation of cathelicidin ll37 expression and nf κb signaling |
| topic | Mycobacterium bovis sodium butyrate histone deacetylation Nuclear factor-κB cathelicidin |
| url | https://www.frontiersin.org/article/10.3389/fmicb.2020.00433/full |
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