Disease Tolerance Mechanisms in Inflammatory Responses
Summary
Inflammatory responses are essential for host defence but can drive collateral tissue damage when uncontrolled. Host strategies to combat infection encompass pathogen resistance, which eliminates or restricts microbial replication, and disease tolerance, which maintains tissue integrity without necessarily reducing pathogen load. Tolerance mechanisms include activation of cytoprotective programmes such as DNA damage responses and autophagy, modulation of metabolic pathways to support antioxidant production, and orchestration of repair processes that restore homeostasis. Organ-specific adaptations—ranging from specialised epithelial regeneration in the lung to metabolic realignment in the liver—further underpin resilience to inflammatory stress. Understanding these diverse mechanisms offers new avenues for therapies aimed at boosting host resilience in sepsis, respiratory infections and chronic inflammatory diseases.
Research from Nature Portfolio
Recent studies have delineated universal patterns of acute inflammatory recovery by tracking longitudinal changes in circulating cell counts across trauma, ischaemia and infection. A conserved trajectory characterised by rapid decline of white blood cell numbers alongside a delayed, linear rise in platelet counts has emerged as a fundamental tolerance mechanism, reflecting coordinated regulation of immune resolution and haemostatic repair. Departures from this co-regulatory dynamic are predictive of adverse outcomes in settings such as cardiac surgery, severe viral infection and sepsis, highlighting the prognostic and therapeutic potential of modulating innate immune kinetics to enhance tolerance.
Disease Tolerance Mechanisms in Inflammatory Responses publication trend
The graph below shows the total number of articles in disease tolerance mechanisms in inflammatory responses across all publications each year (not limited to Nature Index journals).
Technical terms
Disease tolerance: A host defence strategy that limits the negative impact of infection on tissue function without reducing pathogen burden.
Pathogen resistance: Immune mechanisms that detect and eliminate invading microorganisms to decrease pathogen load.
Metabolic reprogramming: The adjustment of cellular metabolic pathways to meet altered energy and biosynthetic demands during stress or infection.
Autophagy: A regulated process of cellular self-digestion that removes damaged organelles and proteins, supporting survival under stress.
References
- Anthracyclines Induce DNA Damage Response-Mediated Protection against Severe Sepsis. Immunity (2013).
- Human acute inflammatory recovery is defined by co-regulatory dynamics of white blood cell and platelet populations. Nature Communications (2022).
- Tissue-specific reprogramming of glutamine metabolism maintains tolerance to sepsis. PLOS ONE (2023).
- Disease tolerance: a protective mechanism of lung infections. Frontiers in Cellular and Infection Microbiology (2023).
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