Abstract
A healthy body activates the immune response to target invading pathogens (i.e. viruses, bacteria, fungi, and parasites) and avoid further systemic infection. The activation of immunological mechanisms includes several components of the immune system, such as innate and acquired immunity. Once any component of the immune response to infections is aberrantly altered or dysregulated, resulting in a failure to clear infection, sepsis will develop through a pro-inflammatory immunological mechanism. Furthermore, the severe inflammatory responses induced by sepsis also increase vascular permeability, leading to acute pulmonary edema and resulting in acute respiratory distress syndrome (ARDS). Apparently, potential for improvement exists in the management of the transition from sepsis to ARDS; thus, this article presents an exhaustive review that highlights the previously unrecognized relationship between sepsis and ARDS and suggests a direction for future therapeutic developments, including plasma and genetic pre-diagnostic strategies and interference with proinflammatory signaling.
Highlights
Due to the development of both overactivation of the innate immune response and immunosuppression, sepsis is considered a medical emergency characterized by severe immune dysregulation with a very complex immunopathogenesis
NAD(P)H: quinone oxidoreductase 1 (NQO1); In a rat model of sepsis-associated acute respiratory distress syndrome (ARDS), the up-regulation of miR-494 decreased the expression of the antioxidant factor NQO1 and inactivated the Nrf2 signaling pathway, which were responsible for significantly higher levels of IL-1β, IL-6, and tumor necrosis factor (TNF)-α, suggesting a pro-inflammatory effect of miR-494 on sepsis-associated ARDS [48]
Mitogen-activated protein kinase (MAPK) signaling is suppressed by blocking the phosphorylation of Jun N-terminal kinase (JNK) and p38, which decreases the levels of the pro-inflammatory cytokines IL-6 and TNF-α and increases the level of the anti-inflammatory cytokine IL-10 to subsequently alleviate the inflammation in subjects with sepsis-induced ARDS [54]
Summary
Due to the development of both overactivation of the innate immune response and immunosuppression, sepsis is considered a medical emergency characterized by severe immune dysregulation with a very complex immunopathogenesis. Consistent with the updated definition of sepsis by the NIH NHLBI Panel, who consider it a severe endothelial dysfunction syndrome induced by intravascular and extravascular infections that lead to reversible or irreversible injury to the microcirculation, ARDS is one stage in the process of multiple organ failure characterized by the increased permeability of pulmonary epithelial and capillary endothelial cells, the influx of large numbers of alveolar macrophages and neutrophils and cell apoptosis [24].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
