Oxidative Stress and Inflammatory Response Mechanisms in Sepsis

Sepsis arises from a dysregulated host response to infection, in which an initial wave of pathogen‐induced inflammation becomes amplified by excessive production of reactive oxygen species (ROS). Mitochondrial dysfunction and activation of immune cells such as neutrophils and macrophages drive oxidative damage to lipids, proteins and nucleic acids, compromising endothelial integrity and promoting microvascular dysfunction. Concurrently, the assembly of inflammasomes accelerates the maturation of interleukins and amplifies cytokine release, prompting a self‐sustaining “cytokine storm.” This inflammatory cascade culminates in multiple organ dysfunction through mechanisms that include endothelial barrier breakdown, aberrant coagulation and immunosuppression. Understanding the cross‐talk between oxidative and inflammatory pathways has underpinned the development of therapeutic strategies aimed at restoring redox balance, modulating innate immunity and preserving organ function. Clinical priorities now include the identification of time‐resolved biomarkers to stratify patients for targeted interventions, alongside novel agents capable of scavenging ROS or inhibiting key inflammatory complexes without exacerbating immunosuppression.

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Oxidative Stress and Inflammatory Response Mechanisms in Sepsis publication trend

The graph below shows the total number of articles in oxidative stress and inflammatory response mechanisms in sepsis across all publications each year (not limited to Nature Index journals).

Technical terms

Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen that, in excess, inflict oxidative damage and also serve as signalling mediators in inflammation.

Cytokines: Small protein messengers secreted by immune cells that orchestrate inflammatory and anti‐inflammatory responses.

Inflammasome: A multiprotein complex that activates inflammatory caspases, leading to maturation and release of interleukins such as IL-1β and IL-18.

Macrophage polarization: The process by which macrophages adopt a proinflammatory (M1) or anti‐inflammatory (M2) phenotype in response to environmental cues.

Biomarker: A measurable indicator of biological processes or pathological states used to guide diagnosis, prognosis and therapeutic decision-making.

References

1. Enhancing sepsis biomarker development: key considerations from public and private perspectives. Critical Care (2024).
2. Potential therapeutic implications of calcitriol administration and weight reduction on CD4 T cell dysregulation and renin angiotensin system-associated acute lung injury in septic obese mice. Biomedicine & Pharmacotherapy (2023).
3. Intratracheal Administration of Stem Cell Membrane-Cloaked Naringin-Loaded Biomimetic Nanoparticles Promotes Resolution of Acute Lung Injury. Antioxidants (2024).
4. Reactive Oxygen Species Interact With NLRP3 Inflammasomes and Are Involved in the Inflammation of Sepsis: From Mechanism to Treatment of Progression. Frontiers in Physiology (2020).