In the development of sepsis following acute insults, the subsets and functions of immune cells appear to be dramatically shifted. In recent years, advanced analytical technologies have identified new immune cell subsets (e.g. innate lymphoid cells), which, despite occurring in relatively low numbers, play a critical role in modulating host immune response and multiple organ dysfunction in sepsis. Many cell subsets begin to differentiate and/or expand shortly after microbial challenge contributing to the immune deregulation. Along with the alterations of immune cell subsets, also induction of various cytokines is critical in mediating immune function. Newly discovered cytokines and mediators contributing to abnormal immunity as well as classic cytokines and chemokines exhibiting newly exposed immunosuppressive properties will be the focus in the pathogenesis of septic complications.
The role and functionality of known and novel inflammatory mediators and immune-inflammatory cells with a potential capacity for indirect and direct immunomodulation require diligent investigation to facilitate a better understanding of the pathogenesis of sepsis.
The goal of this Research Topic is to compile Original Research, Methods, Opinion, Perspective, Mini Review and Review articles expanding knowledge on various mechanistic aspects of sepsis-induced immune-inflammatory deregulation and organ dysfunction. This Research Topic pays special attention to works characterizing: i) any novel immune cell subsets and/or newly discovered inflammatory mediators, and ii) previously unknown and poorly characterized functions and mechanisms exhibited by well-known immune cells and/or inflammatory mediators. Other closely related study topics are also invited and will be considered.
We welcome the submission of Original Research, Methods, Opinion, Perspective, Mini Review and Reviews articles, that cover, but are not limited to, the following topics:
• The role and significance of new subtypes of immune cells and mediators in sepsis-induced immune-deregulation and single/multiple organ dysfunction
• Epigenetic and transcriptomic (as well as other omics approaches) characterization of novel and previously known subtypes of immune cells that are responsible for immune deregulation and organ dysfunction under septic challenge
• Characterization of expression patterns across different phases (acute, chronic), magnitudes (hyper- and hypo-responders) and outcomes (low/high risk of death) of sepsis
• Signaling pathways and immunomodulation for host immune disorder in sepsis
• New functions and/or modulatory signaling of traditional immune cells and mediators known to contribute to the dysregulation of the immuno-inflammatory responses and organ injury in sepsis
In the development of sepsis following acute insults, the subsets and functions of immune cells appear to be dramatically shifted. In recent years, advanced analytical technologies have identified new immune cell subsets (e.g. innate lymphoid cells), which, despite occurring in relatively low numbers, play a critical role in modulating host immune response and multiple organ dysfunction in sepsis. Many cell subsets begin to differentiate and/or expand shortly after microbial challenge contributing to the immune deregulation. Along with the alterations of immune cell subsets, also induction of various cytokines is critical in mediating immune function. Newly discovered cytokines and mediators contributing to abnormal immunity as well as classic cytokines and chemokines exhibiting newly exposed immunosuppressive properties will be the focus in the pathogenesis of septic complications.
The role and functionality of known and novel inflammatory mediators and immune-inflammatory cells with a potential capacity for indirect and direct immunomodulation require diligent investigation to facilitate a better understanding of the pathogenesis of sepsis.
The goal of this Research Topic is to compile Original Research, Methods, Opinion, Perspective, Mini Review and Review articles expanding knowledge on various mechanistic aspects of sepsis-induced immune-inflammatory deregulation and organ dysfunction. This Research Topic pays special attention to works characterizing: i) any novel immune cell subsets and/or newly discovered inflammatory mediators, and ii) previously unknown and poorly characterized functions and mechanisms exhibited by well-known immune cells and/or inflammatory mediators. Other closely related study topics are also invited and will be considered.
We welcome the submission of Original Research, Methods, Opinion, Perspective, Mini Review and Reviews articles, that cover, but are not limited to, the following topics:
• The role and significance of new subtypes of immune cells and mediators in sepsis-induced immune-deregulation and single/multiple organ dysfunction
• Epigenetic and transcriptomic (as well as other omics approaches) characterization of novel and previously known subtypes of immune cells that are responsible for immune deregulation and organ dysfunction under septic challenge
• Characterization of expression patterns across different phases (acute, chronic), magnitudes (hyper- and hypo-responders) and outcomes (low/high risk of death) of sepsis
• Signaling pathways and immunomodulation for host immune disorder in sepsis
• New functions and/or modulatory signaling of traditional immune cells and mediators known to contribute to the dysregulation of the immuno-inflammatory responses and organ injury in sepsis
