sdrH enhances Staphylococcus aureus infection in diabetic wounds
IntroductionDiabetes mellitus is a widespread chronic condition that can lead to a variety of complications. Among the numerous complications associated with diabetes, diabetic foot ulcers are particularly notable due to their high prevalence and potential severity. These ulcers are characterized by...
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Frontiers Media S.A.
2025-06-01
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| Series: | Frontiers in Microbiology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fmicb.2025.1502428/full |
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| author | Kaiyu Nie Kaiyu Nie Kaiyu Nie Kaiyu Wang Kaiyu Wang Yin Wen Yin Wen Jinmei Peng Jinmei Peng Shijie Tang Shijie Tang Shijie Tang |
| author_facet | Kaiyu Nie Kaiyu Nie Kaiyu Nie Kaiyu Wang Kaiyu Wang Yin Wen Yin Wen Jinmei Peng Jinmei Peng Shijie Tang Shijie Tang Shijie Tang |
| author_sort | Kaiyu Nie |
| collection | DOAJ |
| description | IntroductionDiabetes mellitus is a widespread chronic condition that can lead to a variety of complications. Among the numerous complications associated with diabetes, diabetic foot ulcers are particularly notable due to their high prevalence and potential severity. These ulcers are characterized by a substantial incidence rate, a considerable risk of infection, and a high probability of necessitating amputation. Staphylococcus aureus, a notorious pathogen within this context, exacerbates wound pathogenesis and can facilitate ulcer extension and, in severe instances, gangrene through the secretion of numerous virulence factors.MethodsRT–qPCR was used to analyze the expression of Staphylococcus aureus adhesin virulence factors. Utilizing gene knockout techniques to deleted the sdrH and icaA-C genes. Biofilm formation of S. aureus was observed by scanning electron microscope. The effect of sdrH and icaA-C genes on S. aureus infected wound healing was also evaluated using a diabetic mice skin wound infection model.ResultsThe sdrH gene and the icaA-C gene cluster are critical contributors to Staphylococcus aureus infection in diabetic wounds. Post-infection with the sdrH single-gene knockout strain, a significant enhancement in wound healing rates was observed, accompanied by a marked reduction in bacterial colonization per unit area. Conversely, no significant differences were detected between the icaA-C gene cluster knockout strain and the wild-type strain. Compared to infections caused by either the wild-type strain or the sdrH single-knockout strain, infection with the icaA-C/sdrH double-knockout strain led to a marked increase in the wound healing rate and a significant reduction in bacterial load.DiscussionThis study presented that the sdrH gene enhances the virulence of Staphylococcus aureus in diabetic wounds by attenuating the host immune response, reducing the infiltration of inflammatory cells, and impairing the immune system’s capacity to clear bacteria, thereby impeding the wound healing process. Although icaA-C is not a pivotal player, it seems to enhance the virulence capabilities of sdrH. |
| format | Article |
| id | doaj-art-e79e8f36a27e4ab0949d9e1be6b8f014 |
| institution | DOAJ |
| issn | 1664-302X |
| language | English |
| publishDate | 2025-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Microbiology |
| spelling | doaj-art-e79e8f36a27e4ab0949d9e1be6b8f0142025-08-20T03:21:59ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2025-06-011610.3389/fmicb.2025.15024281502428sdrH enhances Staphylococcus aureus infection in diabetic woundsKaiyu Nie0Kaiyu Nie1Kaiyu Nie2Kaiyu Wang3Kaiyu Wang4Yin Wen5Yin Wen6Jinmei Peng7Jinmei Peng8Shijie Tang9Shijie Tang10Shijie Tang11Department of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, ChinaPlastic Surgery Institute of Shantou University Medical College, Guangzhou, ChinaShantou Plastic Surgery Clinical Research Center, Guangzhou, ChinaDepartment of Burns and Plastic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaThe Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, ChinaDepartment of Burns and Plastic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaThe Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, ChinaDepartment of Burns and Plastic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, ChinaThe Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University, Zunyi, ChinaDepartment of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College, Shantou, Guangdong, ChinaPlastic Surgery Institute of Shantou University Medical College, Guangzhou, ChinaShantou Plastic Surgery Clinical Research Center, Guangzhou, ChinaIntroductionDiabetes mellitus is a widespread chronic condition that can lead to a variety of complications. Among the numerous complications associated with diabetes, diabetic foot ulcers are particularly notable due to their high prevalence and potential severity. These ulcers are characterized by a substantial incidence rate, a considerable risk of infection, and a high probability of necessitating amputation. Staphylococcus aureus, a notorious pathogen within this context, exacerbates wound pathogenesis and can facilitate ulcer extension and, in severe instances, gangrene through the secretion of numerous virulence factors.MethodsRT–qPCR was used to analyze the expression of Staphylococcus aureus adhesin virulence factors. Utilizing gene knockout techniques to deleted the sdrH and icaA-C genes. Biofilm formation of S. aureus was observed by scanning electron microscope. The effect of sdrH and icaA-C genes on S. aureus infected wound healing was also evaluated using a diabetic mice skin wound infection model.ResultsThe sdrH gene and the icaA-C gene cluster are critical contributors to Staphylococcus aureus infection in diabetic wounds. Post-infection with the sdrH single-gene knockout strain, a significant enhancement in wound healing rates was observed, accompanied by a marked reduction in bacterial colonization per unit area. Conversely, no significant differences were detected between the icaA-C gene cluster knockout strain and the wild-type strain. Compared to infections caused by either the wild-type strain or the sdrH single-knockout strain, infection with the icaA-C/sdrH double-knockout strain led to a marked increase in the wound healing rate and a significant reduction in bacterial load.DiscussionThis study presented that the sdrH gene enhances the virulence of Staphylococcus aureus in diabetic wounds by attenuating the host immune response, reducing the infiltration of inflammatory cells, and impairing the immune system’s capacity to clear bacteria, thereby impeding the wound healing process. Although icaA-C is not a pivotal player, it seems to enhance the virulence capabilities of sdrH.https://www.frontiersin.org/articles/10.3389/fmicb.2025.1502428/fulldiabetes mellitusdiabetic ulcerStaphylococcus aureusinfectionvirulence factors |
| spellingShingle | Kaiyu Nie Kaiyu Nie Kaiyu Nie Kaiyu Wang Kaiyu Wang Yin Wen Yin Wen Jinmei Peng Jinmei Peng Shijie Tang Shijie Tang Shijie Tang sdrH enhances Staphylococcus aureus infection in diabetic wounds Frontiers in Microbiology diabetes mellitus diabetic ulcer Staphylococcus aureus infection virulence factors |
| title | sdrH enhances Staphylococcus aureus infection in diabetic wounds |
| title_full | sdrH enhances Staphylococcus aureus infection in diabetic wounds |
| title_fullStr | sdrH enhances Staphylococcus aureus infection in diabetic wounds |
| title_full_unstemmed | sdrH enhances Staphylococcus aureus infection in diabetic wounds |
| title_short | sdrH enhances Staphylococcus aureus infection in diabetic wounds |
| title_sort | sdrh enhances staphylococcus aureus infection in diabetic wounds |
| topic | diabetes mellitus diabetic ulcer Staphylococcus aureus infection virulence factors |
| url | https://www.frontiersin.org/articles/10.3389/fmicb.2025.1502428/full |
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