Abstract:In bacteria, DegS protease functions as an activating factor of the σE envelope stress response system, which ultimately activates the transcription of stress response genes in the cytoplasm. On the basis of high-throughput RNA sequencing, we have previously found that degS knockout inhibits the expression of flagellum synthesis- and chemotaxis-related genes, thereby indicating that DegS may be involved in the regulation of V. cholerae motility. In this study, we examined the relationships between DegS and mot… Show more
“…Compared with the NAC-group, the ability of the DdegS, DrpoE, and DrpoS strains to colonize the mouse intestine could be partially restored after the reduction of oxidative stress in the NAC+ group, but not to a level close to that of the wild-type, suggesting that adaptation to the oxidative stress environment is only a part of the V. cholerae's ability to colonize the intestine. The main reason for this is that in NAC untreated, the DdegS, DrpoE, and DrpoS mutant strains significantly reduced V. cholerae's ability to colonize the mice intestine, which is in agreement with our previous findings (Zou et al, 2023). However, in the present study, we also found that with and without NAC treatment, WT, DdegS:: degS, DdegSDrseA, DdegS+ pBAD24-rpoS, and DdegS+ pBAD24-xthA strains did not differ significantly in their ability to colonize the gut.…”
Section: Discussionsupporting
confidence: 92%
“…Compared with the NAC untreated group, the colonization ability of the ΔdegS strain increased after NAC treatment, while there was no significant difference in the colonization ability of the ΔdegS +pBAD24- xthA strain, suggesting that the diminished colonization ability of the ΔdegS strain was only partially affected by the oxidative stress environment. XthA overexpression could eliminate the influence of oxidative stress, and could not revert to the influence of other factors, including motility, chemotaxis on intestinal colonization ( Zou et al., 2023 ).The differences with the Davies study may be due to the different strains we used and the different mice models.…”
Section: Discussionmentioning
confidence: 97%
“…The cAMP-CRP-RpoS pathway plays an essential role in oxidative stress in Salmonella (Cheng and Sun, 2009). Our previous results showed that DegS regulated V.cholerae motility and chemotaxis via cAMP-CRP-RpoS-FlhF pathway (Zou et al, 2023).In the present study, we investigated the effect of DegS on the antioxidant capacity of V.cholerae. Our results show that DegS regulates the expression of the nucleic acid exonuclease III gene xthA through the cAMP-CRP-RpoS pathway, thereby affecting the antioxidant capacity of V.cholerae.…”
Adaptation to oxidative stress is critical for survival of Vibrio cholerae in aquatic ecosystems and hosts. DegS activates the σE envelope stress response. We have previously revealed that DegS may be involved in regulating the oxidative stress response. In this study, we demonstrated that deletion of the degS gene attenuates the antioxidant capacity of V. cholerae. In addition, our results further revealed that the regulation of antioxidant capacity by DegS in V. cholerae could involve the cAMP-CRP complex, which regulates rpoS. XthA is an exonuclease that repairs oxidatively damaged cells and affects the bacterial antioxidant capacity. qRT-PCR showed that DegS, σE, cAMP, CRP, and RpoS positively regulate xthA gene transcription. XthA overexpression partially compensates for antioxidant deficiency in the degS mutant. These results suggest that DegS affects the antioxidant capacity of V.cholerae by regulating xthA expression via the cAMP-CRP-RpoS pathway. In a mouse intestinal colonization experiment, our data showed that V.cholerae degS, rpoE, and rpoS gene deletions were associated with significantly reduced resistance to oxidative stress and the ability to colonize the mouse intestine. In conclusion, these findings provide new insights into the regulation of antioxidant activity by V.cholerae DegS.
“…Compared with the NAC-group, the ability of the DdegS, DrpoE, and DrpoS strains to colonize the mouse intestine could be partially restored after the reduction of oxidative stress in the NAC+ group, but not to a level close to that of the wild-type, suggesting that adaptation to the oxidative stress environment is only a part of the V. cholerae's ability to colonize the intestine. The main reason for this is that in NAC untreated, the DdegS, DrpoE, and DrpoS mutant strains significantly reduced V. cholerae's ability to colonize the mice intestine, which is in agreement with our previous findings (Zou et al, 2023). However, in the present study, we also found that with and without NAC treatment, WT, DdegS:: degS, DdegSDrseA, DdegS+ pBAD24-rpoS, and DdegS+ pBAD24-xthA strains did not differ significantly in their ability to colonize the gut.…”
Section: Discussionsupporting
confidence: 92%
“…Compared with the NAC untreated group, the colonization ability of the ΔdegS strain increased after NAC treatment, while there was no significant difference in the colonization ability of the ΔdegS +pBAD24- xthA strain, suggesting that the diminished colonization ability of the ΔdegS strain was only partially affected by the oxidative stress environment. XthA overexpression could eliminate the influence of oxidative stress, and could not revert to the influence of other factors, including motility, chemotaxis on intestinal colonization ( Zou et al., 2023 ).The differences with the Davies study may be due to the different strains we used and the different mice models.…”
Section: Discussionmentioning
confidence: 97%
“…The cAMP-CRP-RpoS pathway plays an essential role in oxidative stress in Salmonella (Cheng and Sun, 2009). Our previous results showed that DegS regulated V.cholerae motility and chemotaxis via cAMP-CRP-RpoS-FlhF pathway (Zou et al, 2023).In the present study, we investigated the effect of DegS on the antioxidant capacity of V.cholerae. Our results show that DegS regulates the expression of the nucleic acid exonuclease III gene xthA through the cAMP-CRP-RpoS pathway, thereby affecting the antioxidant capacity of V.cholerae.…”
Adaptation to oxidative stress is critical for survival of Vibrio cholerae in aquatic ecosystems and hosts. DegS activates the σE envelope stress response. We have previously revealed that DegS may be involved in regulating the oxidative stress response. In this study, we demonstrated that deletion of the degS gene attenuates the antioxidant capacity of V. cholerae. In addition, our results further revealed that the regulation of antioxidant capacity by DegS in V. cholerae could involve the cAMP-CRP complex, which regulates rpoS. XthA is an exonuclease that repairs oxidatively damaged cells and affects the bacterial antioxidant capacity. qRT-PCR showed that DegS, σE, cAMP, CRP, and RpoS positively regulate xthA gene transcription. XthA overexpression partially compensates for antioxidant deficiency in the degS mutant. These results suggest that DegS affects the antioxidant capacity of V.cholerae by regulating xthA expression via the cAMP-CRP-RpoS pathway. In a mouse intestinal colonization experiment, our data showed that V.cholerae degS, rpoE, and rpoS gene deletions were associated with significantly reduced resistance to oxidative stress and the ability to colonize the mouse intestine. In conclusion, these findings provide new insights into the regulation of antioxidant activity by V.cholerae DegS.
“…In addition, many studies have also found that cAMP-CRP could affect the virulence and colonization of V. cholerae through different regulatory ways. For example, according to Zou M. et al, DegS regulates V. cholerae's chemotaxis and motility through the cAMP-CRP-RpoS-FlhF pathway, which has an impact on the colonization of suckling mice intestines [28]. Muzhingi I et al demonstrated that V. cholerae controls the pathogenicity of interactions with arthropod hosts via the activity of the two-component CrbS/R system and cAMP-CRP activates the expression of the crbS and crbR genes [29].…”
Vibrio cholerae is an intestinal pathogen that can cause severe diarrheal disease. The disease has afflicted millions of people since the 19th century and has aroused global concern. The Vibrio Pathogenicity Island-2 (VPI-2) is a 57.3 kb region, VC1758–VC1809, which is present in choleragenic V. cholerae. At present, little is known about the function of VC1795 in the VPI-2 of V. cholerae. In this study, the intestinal colonization ability of the ΔVC1795 strain was significantly reduced compared to that of the wild-type strain, and the colonization ability was restored to the wild-type strain after VC1795 gene replacement. This result indicated that the VC1795 gene plays a key role in the intestinal colonization and pathogenicity of V. cholerae. Then, we explored the upstream and downstream regulation mechanisms of the VC1795 gene. Cyclic adenylate receptor protein (CRP) was identified as being located upstream of VC1795 by a DNA pull-down assay and electrophoretic mobility shift assays (EMSAs) and negatively regulating the expression of VC1795. In addition, the results of Chromatin immunoprecipitation followed by sequencing (ChIP-seq), EMSAs, and Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) indicated that VC1795 directly negatively regulates the expression of its downstream gene, VC1794. Furthermore, by using qRT-PCR, we hypothesized that VC1795 indirectly positively regulates the toxin-coregulated pilus (TCP) cluster to influence the colonization ability of V. cholerae in intestinal tracts. In short, our findings support the key regulatory role of VC1795 in bacterial pathogenesis as well as lay the groundwork for the further determination of the complex regulatory network of VC1795 in bacteria.
“…The “ggplot2” R package was utilized to create a volcano plot, which illustrates the results. Furthermore, the “pheatmap” R package was employed to perform a bidirectional hierarchical clustering analysis of the collected DEGs (Xiantao tool, www.xiantao.com ) ( 12 ).…”
BackgroundTregs plays a critical role in the development of secondary injuries in diseases. Accumulating evidence suggests an association between ischemic stroke and renal dysfunction; however, the underlying mechanisms remain unclear. This study aimed to investigate the potential of Tregs in inhibiting the activation of astrocytes after focal cerebral infarction.MethodsThis study aimed to investigate the renal consequences of focal cerebral ischemia by subjecting a mouse model to transient middle cerebral artery occlusion (tMCAO). Subsequently, we assessed renal fibrosis, renal ferroptosis, Treg infiltration, astrocyte activation, as well as the expression levels of active GPX4, FSP1, IL-10, IL-6, and IL-2 after a 2-week period.ResultsIn the tMCAO mouse model, depletion of tregs protected against activation of astrocyte and significantly decreased FSP1, IL-6, IL-2, and NLRP3 expression levels, while partially reversing the changes in Tregs. Mechanistically, tregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.ConclusionTregs depletion attenuates renal fibrosis by modulating IL-10/GPX4 following cerebral infarction.
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