sdrH enhances Staphylococcus aureus infection in diabetic wounds
Diabetes 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 substanti...
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Published in | Frontiers in microbiology Vol. 16; p. 1502428 |
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Abstract | Diabetes 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.
, 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.
RT-qPCR was used to analyze the expression of
adhesin virulence factors. Utilizing gene knockout techniques to deleted the
and
genes. Biofilm formation of S. aureus was observed by scanning electron microscope. The effect of
and
genes on
infected wound healing was also evaluated using a diabetic mice skin wound infection model.
The
gene and the
gene cluster are critical contributors to
infection in diabetic wounds. Post-infection with the
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
gene cluster knockout strain and the wild-type strain. Compared to infections caused by either the wild-type strain or the
single-knockout strain, infection with the
/
double-knockout strain led to a marked increase in the wound healing rate and a significant reduction in bacterial load.
This study presented that the
gene enhances the virulence of
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
is not a pivotal player, it seems to enhance the virulence capabilities of
. |
---|---|
AbstractList | Diabetes 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.
, 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.
RT-qPCR was used to analyze the expression of
adhesin virulence factors. Utilizing gene knockout techniques to deleted the
and
genes. Biofilm formation of S. aureus was observed by scanning electron microscope. The effect of
and
genes on
infected wound healing was also evaluated using a diabetic mice skin wound infection model.
The
gene and the
gene cluster are critical contributors to
infection in diabetic wounds. Post-infection with the
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
gene cluster knockout strain and the wild-type strain. Compared to infections caused by either the wild-type strain or the
single-knockout strain, infection with the
/
double-knockout strain led to a marked increase in the wound healing rate and a significant reduction in bacterial load.
This study presented that the
gene enhances the virulence of
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
is not a pivotal player, it seems to enhance the virulence capabilities of
. Diabetes 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.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.RT-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.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.The 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.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.This 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.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. 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. |
Author | Wang, Kaiyu Nie, Kaiyu Tang, Shijie Wen, Yin Peng, Jinmei |
AuthorAffiliation | 3 Shantou Plastic Surgery Clinical Research Center , Guangzhou , China 1 Department of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College , Shantou, Guangdong , China 4 Department of Burns and Plastic Surgery, Affiliated Hospital of Zunyi Medical University , Zunyi , China 2 Plastic Surgery Institute of Shantou University Medical College , Guangzhou , China 5 The Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University , Zunyi , China |
AuthorAffiliation_xml | – name: 4 Department of Burns and Plastic Surgery, Affiliated Hospital of Zunyi Medical University , Zunyi , China – name: 1 Department of Plastic Surgery and Burn Center, Second Affiliated Hospital, Shantou University Medical College , Shantou, Guangdong , China – name: 2 Plastic Surgery Institute of Shantou University Medical College , Guangzhou , China – name: 3 Shantou Plastic Surgery Clinical Research Center , Guangzhou , China – name: 5 The Collaborative Innovation Center of Tissue Damage Repair and Regeneration Medicine of Zunyi Medical University , Zunyi , China |
Author_xml | – sequence: 1 givenname: Kaiyu surname: Nie fullname: Nie, Kaiyu – sequence: 2 givenname: Kaiyu surname: Wang fullname: Wang, Kaiyu – sequence: 3 givenname: Yin surname: Wen fullname: Wen, Yin – sequence: 4 givenname: Jinmei surname: Peng fullname: Peng, Jinmei – sequence: 5 givenname: Shijie surname: Tang fullname: Tang, Shijie |
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Keywords | infection diabetes mellitus diabetic ulcer Staphylococcus aureus virulence factors |
Language | English |
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