IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR
Abstract Human papillomavirus (HPV) is the most prevalent sexually transmitted infection globally, with significant implications for various anogenital cancers, such as vulval, vaginal, anal, penile, head and neck cancers. HPV infections have been linked to the induction of inflammation. In contrast...
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| Format: | Article |
| Language: | English |
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BMC
2024-12-01
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| Series: | Virology Journal |
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| Online Access: | https://doi.org/10.1186/s12985-024-02615-4 |
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| author | Yahong Shi Ning Liu Yunfang Bai Kunshan Li Chencong Li Yujiao Hou |
| author_facet | Yahong Shi Ning Liu Yunfang Bai Kunshan Li Chencong Li Yujiao Hou |
| author_sort | Yahong Shi |
| collection | DOAJ |
| description | Abstract Human papillomavirus (HPV) is the most prevalent sexually transmitted infection globally, with significant implications for various anogenital cancers, such as vulval, vaginal, anal, penile, head and neck cancers. HPV infections have been linked to the induction of inflammation. In contrast, Interleukin-37 (IL-37) is recognized as an anti-inflammatory cytokine. In this study, two distinct types of oral epithelial cells were employed to investigate the impact of HPV on inflammation. The experimental outcomes unequivocally demonstrated that human papillomavirus (HPV) elicited a pronounced and statistically significant induction of inflammatory responses within both varieties of oral epithelial cells under investigation. Interestingly, IL-37 exhibited a mitigating effect, attenuating the HPV-induced inflammation in oral epithelial cells. Further exploration into the molecular mechanisms involved revealed that knockdown (KD) of PI3K compromised the anti-inflammatory effects of IL-37 in response to HPV. Similarly, KD of AKT was found to compromise the regulatory effects of IL-37 on HPV-induced inflammation. Notably, KD of mTOR was identified as a key factor, compromising the anti-inflammatory effects of IL-37 in the context of HPV-induced inflammation. Additionally, the study uncovered that the mTOR inhibitor, rapamycin, could effectively compromise the effects of IL-37 on HPV-induced inflammation. These findings contribute valuable insights into the intricate pathogenesis of HPV-induced inflammation and may pave the way for the development of innovative treatments for this condition. |
| format | Article |
| id | doaj-art-9eb78d6f6d3840cfa8cd68529bff430c |
| institution | Kabale University |
| issn | 1743-422X |
| language | English |
| publishDate | 2024-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Virology Journal |
| spelling | doaj-art-9eb78d6f6d3840cfa8cd68529bff430c2025-01-05T12:08:31ZengBMCVirology Journal1743-422X2024-12-0121111310.1186/s12985-024-02615-4IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTORYahong Shi0Ning Liu1Yunfang Bai2Kunshan Li3Chencong Li4Yujiao Hou5Department of Stomatology, Second Hospital of ShijiazhuangDepartment of Endoscopy, The Fourth Hospital of Hebei Medical UniversityDepartment of Emergency, The Fourth Hospital of Hebei Medical UniversityDepartment of Stomatology, The Fourth Hospital of Hebei Medical UniversityPhysical Examination Center, The Fourth Hospital of Hebei Medical UniversityDepartment of Stomatology, Affiliated Hospital of Hebei UniversityAbstract Human papillomavirus (HPV) is the most prevalent sexually transmitted infection globally, with significant implications for various anogenital cancers, such as vulval, vaginal, anal, penile, head and neck cancers. HPV infections have been linked to the induction of inflammation. In contrast, Interleukin-37 (IL-37) is recognized as an anti-inflammatory cytokine. In this study, two distinct types of oral epithelial cells were employed to investigate the impact of HPV on inflammation. The experimental outcomes unequivocally demonstrated that human papillomavirus (HPV) elicited a pronounced and statistically significant induction of inflammatory responses within both varieties of oral epithelial cells under investigation. Interestingly, IL-37 exhibited a mitigating effect, attenuating the HPV-induced inflammation in oral epithelial cells. Further exploration into the molecular mechanisms involved revealed that knockdown (KD) of PI3K compromised the anti-inflammatory effects of IL-37 in response to HPV. Similarly, KD of AKT was found to compromise the regulatory effects of IL-37 on HPV-induced inflammation. Notably, KD of mTOR was identified as a key factor, compromising the anti-inflammatory effects of IL-37 in the context of HPV-induced inflammation. Additionally, the study uncovered that the mTOR inhibitor, rapamycin, could effectively compromise the effects of IL-37 on HPV-induced inflammation. These findings contribute valuable insights into the intricate pathogenesis of HPV-induced inflammation and may pave the way for the development of innovative treatments for this condition.https://doi.org/10.1186/s12985-024-02615-4HPVIL-37InflammationGrowthOral epithelial cells |
| spellingShingle | Yahong Shi Ning Liu Yunfang Bai Kunshan Li Chencong Li Yujiao Hou IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR Virology Journal HPV IL-37 Inflammation Growth Oral epithelial cells |
| title | IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR |
| title_full | IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR |
| title_fullStr | IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR |
| title_full_unstemmed | IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR |
| title_short | IL-37 attenuated HPV induced inflammation of oral epithelial cells via inhibiting PI3K/AKT/mTOR |
| title_sort | il 37 attenuated hpv induced inflammation of oral epithelial cells via inhibiting pi3k akt mtor |
| topic | HPV IL-37 Inflammation Growth Oral epithelial cells |
| url | https://doi.org/10.1186/s12985-024-02615-4 |
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