Transcriptomic Profiling on Intestine of Diabetic and Septic Mice [RNA-seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE319453 | GEO | 2026/02/20
REPOSITORIES: GEO
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Project description:Sepsis is a severe clinical syndrome related to an exaggerated host immune response to infection as well as systematic inflammation and serious tissue damage. Sepsis-associated acute kidney injury (SA-AKI) is one of the most frequent and serious complications of sepsis. This study aimed to identify new mechanisms in SA-AKI through transcriptome profiling (RNA-seq).
2022-08-17 | GSE186822 | GEO
Project description:Sepsis is the most common cause of hospitalization worldwide. Millions of people survive sepsis each year and are at risk for rehospitalization and death. Pulmonary complications such as respiratory failure due to pneumonia and exacerbation of chronic respiratory disease are among the most common reasons for rehospitalization in sepsis survivors. In order to prevent additional morbidity and death in patients surviving sepsis, we must establish biomarkers to identify patients at risk for pulmonary complications and develop treatments. Late complications in sepsis survivors, particularly nosocomial infections, are proposed to occur through persistent immune reprogramming after sepsis known as immunoparalysis. However, pro-inflammatory immune reprogramming in the form of primed or enhanced responses to secondary stimuli has also been described and could directly contribute to tissue injury and death. Primed immune responses and their contribution to long-term sepsis complications remains understudied. We hypothesize that primed immune responses to inflammatory stimuli in the lung after sepsis are associated with pulmonary complications in survivors of sepsis. To this end, we developed a model of antibiotic treated sepsis induced by cecal ligation and puncture followed three weeks later by secondary challenge with intranasal lipopolysaccharide to induce inflammatory lung injury. We find that mice surviving sepsis have enhanced lung injury responses in the setting of an exaggerated proinflammatory immune response, including primed Ly6Chi monocyte Tnf expression. Using RNA sequencing, we identified derangements in lung gene expression after CLP prior to LPS administration which may mediate enhanced lung injury in this model. One potential mediator, S100A8/A9, was also found to be elevated in the circulation of human sepsis survivors for up to 180 days after sepsis. These findings validate our model and identify S100A8/A9 as one of many potential biomarkers and therapeutic targets for patients at risk for long-term pulmonary complications after sepsis. The role of S100A8/A9, monocyte priming, and other factors predisposing to enhanced lung injury responses and pulmonary complications after sepsis warrant further investigation in humans and mice.
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Project description:This study investigates the role of DDX3X SUMOylation in the activation of the NLRP3 inflammasome during sepsis. We demonstrate that SUMOylation of DDX3X, regulated by the SUMO protease SENP1, is a crucial trigger for NLRP3 inflammasome activation. In endotoxemia and sepsis models, the absence of SENP1 in macrophages and mice led to increased NLRP3 inflammasome activation. Mechanistically, DDX3X SUMOylation promoted the interaction of NLRP3 at lysine 118, inhibiting K48-conjugated ubiquitination and subsequent degradation of NLRP3 by the deubiquitinase OTUD6A, resulting in enhanced oligomerization of NLRP3. In murine adoptive transfer experiments, macrophages expressing the SUMOylation-inhibiting mutation DDX3X-K118R suppressed NLRP3 inflammasome activation, providing protection against LPS-induced inflammatory lung injury. These findings suggest that SENP1-mediated DDX3X deSUMOylation regulates NLRP3 inflammasome activation, offering a potential therapeutic avenue to mitigate NLRP3-induced inflammation.
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Project description:Background: Sepsis can lead to multiple organ damage, and the heart is one of the most vulnerable organs. Vagal nerve stimulation can reduce myocardial injury in sepsis and improve survival rate. However, the relative effect of disparate cell populations on sepsis induced myocardial dysfunction and the low-level tragus stimulation on it, remain unclear. Methods: We used the cardiac single-cell transcriptomic strategy to characterize the cardiac cell population and the network of cells that forms the heart. And we selected all cardiac macrophage from CD45+ cells using single-cell mRNA sequencing data. Then we used echocardiography performing, western blot and immunofluorescence and immunohistochemical technology to verify the data of the single-cell mRNA sequencing results. Results: In single-cell mRNA sequencing data, our analysis provides a comprehensive map of the cardiac cellular landscape uncovering multiple cell populations that contribute to sepsis induced myocardial dysfunction under low-level tragus stimulation. Pseudo timing analysis in single-cell sequencing showed that low level vagal nerve stimulation could induce the transformation of cardiac monocytes into M2 macrophages and play an anti-inflammatory role. After low-level tragus stimulation, the expression of α7nAChR in the heart tissue increased significantly. Echocardiography showed that low-level tragus stimulation could improve the cardiac function of septic myocardial injury of the mice. Comparing with the sepsis group, the expression of interleukin-1β in heart tissue of the mice in sepsis with low-level tragus stimulation group is significantly lower. Conclusion: Low-level tragus stimulation can improve sepsis-induced myocardial dysfunction by promoting cardiac monocytes to M2 macrophages. Goal of the study: In the present study, we aimed to screen macrophages, their crosstalk with other cells, and macrophages associated with cardiac injury and further verify their origins and roles in the septic myocardial injury process and low-level tragus stimulation (LL-TS) to treat septic myocardial dysfunction.
2022-10-26 | GSE207363 | GEO
Project description:Transcriptomic Profiling on Intestine of Diabetic and Septic Mice [RNA-seq]
| PRJNA1423300 | ENA
Project description:Transcriptomic Profiling on Intestine of Diabetic and Septic Mice [miRNA-seq]
| PRJNA1423320 | ENA
Project description:Cardiac dysfunction is a serious complication of sepsis-induced multiorgan failure in intensive care units and is characterized by an uncontrolled immune response to overwhelming infection. Type 2 innate lymphoid cells (ILC2s), as a part of the innate immune system, play a crucial role in the inflammatory process of heterogeneous cardiac disorders. However, the role of ILC2 in regulating sepsis-induced cardiac dysfunction and its underlying mechanism remain unknown. The present study demonstrated that autophagic flux blockage exacerbated inflammatory response and cardiac dysfunction, which was associated with mortality of sepsis. Using a cecal ligation and puncture (CLP) mouse sepsis model, we observed an expansion of ILC2s in the septic heart. Furthermore, IL-4 derived from ILC2 mitigated cardiac inflammatory responses and improved cardiac function during sepsis. Additionally, IL-4 restored the impaired autophagic flux and enhanced lysosomal-associated membrane protein 2 (LAMP2) expression to stabilize lysosomal homeostasis during sepsis. Notably, LAMP2 preferentially bound to Flotillin2 (FLOT2) after IL-4 exposure and the interaction enhanced autophagosome-lysosome fusion in cardiac endothelial cells. Loss of FLOT2 reversed the regulatory effects of LAMP2 on autophagy mediated by IL-4, leading to autophagosome accumulation and suppressed autophagosome clearance. Conclusively, these findings provide novel insights that ILC2 regulates incomplete autophagic flux to protect septic heart and expand our understanding of immunoregulation for sepsis.
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Project description:Sepsis is characterized by chronic inflammation and immunosuppression, two immune states that hinder effective infection control and significantly contribute to renal pathological damage. Recent studies have underscored the crucial role of splenic neuroimmune interactions in immune response regulation. However, the precise mechanisms and functions of splenic nerve regulation of splenic immune responses in sepsis-associated acute kidney injury (SA-AKI) remain obscure. Our research suggests that preemptive Splenic Denervation in mice can mitigate sepsis-induced renal injury, while local norepinephrine injection into the spleen exacerbates sepsis-induced kidney damage in the cecal ligation and puncture (CLP) mouse model. Targeted blockade of splenic β2-adrenergic receptor signaling leads to increased survival rates and diminished renal damage in the mice treated with CLP. Subsequent experiments involving local splenic administration of Gr-1 antibodies and myeloid cell-specific conditional knockout of Adrb2 in mice validate that during sepsis, NE/β2-AR signaling can impact splenic neutrophils, fostering the progression of acute sepsis. Mechanistic inquiries reveal that splenic Adrb2 signaling boosts neutrophil PGE2 signaling through the cAMP pathway, promoting Th1 activation, diminishing local bacterial infections, and ameliorating SA-AKI. Furthermore, Blocking ADRB2 or PGE2 synthesizing signal significantly modulates the immunosuppression effect of neutrophils, promoting anti-bacterial Th1 immune response. These studies elucidate the role of splenic NE-ADRB2 signaling in regulating neutrophil immunosuppressive functions, thereby influencing the advancement of sepsis and renal tissue damage.
2026-02-17 | GSE289832 | GEO