Points of control in inflammation
Abstract
Inflammation is a complex set of interactions among soluble factors and cells that can arise in any tissue in response to traumatic, infectious, post-ischaemic, toxic or autoimmune injury. The process normally leads to recovery from infection and to healing, However, if targeted destruction and assisted repair are not properly phased, inflammation can lead to persistent tissue damage by leukocytes, lymphocytes or collagen. Inflammation may be considered in terms of its checkpoints, where binary or higher-order signals drive each commitment to escalate, go signals trigger stop signals, and molecules responsible for mediating the inflammatory response also suppress it, depending on timing and context. The non-inflammatory state does not arise passively from an absence of inflammatory stimuli; rather, maintenance of health requires the positive actions of specific gene products to suppress reactions to potentially inflammatory stimuli that do not warrant a full response.
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Without sufficient glucocorticoid regulation, the duration and/or intensity of the inflammatory response increases, heightening risk for acute exacerbations such as occur in asthma and autoimmune diseases, as well as for the onset and progression of chronic inflammatory diseases such as CVD and type II diabetes.
“Without sufficient glucocorticoid regulation, the duration and/or intensity of the inflammatory response increases, heightening risk for acute exacerbations such as occur in asthma and autoimmune diseases, as well as for the onset and progression of chronic inflammatory diseases such as CVD, and type II diabetes (12).”
From Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk (2012) · cites this paper as [12]
Many endogenous antiinflammatory mediators can prevent cytokine-mediated disease.
“Many endogenous antiinflammatory mediators can prevent cytokine-mediated disease (reviewed in ref. 10).”
From Physiology and immunology of the cholinergic antiinflammatory pathway (2007) · cites this paper as [10]
When sufficient concentrations of endogenous antiinflammatory mediators are achieved, proinflammatory cytokine levels are inhibited, the inflammatory response is dampened, and damage is prevented.
“When sufficient concentrations are achieved, proinflammatory cytokine levels are inhibited, the magnitude of the inflammatory response is dampened, and damage is prevented.”
From Physiology and immunology of the cholinergic antiinflammatory pathway (2007) · cites this paper as [10]
High cellular ROS levels are associated with cancer, diabetes, inflammatory diseases, ischemia-related diseases, and neurodegeneration.
“Second, high cellular ROS levels are associated with cancer, diabetes, inflammatory diseases, ischemia-related diseases, and neurodegeneration, and are thus commonly thought to contribute to human pathologies and aging 80–83.”
From Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes (2010) · cites this paper as [83]
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- Authors
- Nathan, C.
- Affiliations
- Cornell University (US)
- Corresponding author
- Nathan, Carl
- ORCID
- Nathan, Carl
- Venue
- Nature
- Published
- 2002-12
- Volume
- 420
- Issue
- 6917
- Pages
- 846-852
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2056879548
- Cited by
- 2,738
- References
- 115
- Citations by year
- 2026: 72 · 2025: 86 · 2024: 117 · 2023: 122 · 2022: 156 · 2021: 141 · 2020: 112 · 2019: 109 · 2018: 113 · 2017: 134 · 2016: 114 · 2015: 128 · 2014: 145 · 2013: 143 · 2012: 128
- FWCI
- 5.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Hearst Foundations
- National Institutes of Health
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- inflammation, inflammatory signaling, anti-inflammatory regulation, tissue damage, leukocytes, lymphocytes, collagen, immune regulation
- MeSH terms
- Animals, Humans, Inflammation, Cytokines, Apoptosis, Oxidative Stress, Genetic Predisposition to Disease
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