Glucocorticoids sensitize the innate immune system through regulation of the NLRP3 inflammasome
Open accessAbstract
Glucocorticoids have long been recognized as powerful anti-inflammatory compounds that are one of the most widely prescribed classes of drugs in the world. However, their role in the regulation of innate immunity is not well understood. We sought to examine the effects of glucocorticoids on the NOD-like receptors (NLRs), a central component of the inflammasome and innate immunity. Surprisingly, we show that glucocorticoids induce both NLRP3 messenger RNA and protein, which is a critical component of the inflammasome. The glucocorticoid-dependent induction of NLRP3 sensitizes the cells to extracellular ATP and significantly enhances the ATP-mediated release of proinflammatory molecules, including mature IL-1β, TNF-α, and IL-6. This effect was specific for glucocorticoids and dependent on the glucocorticoid receptor. These studies demonstrate a novel role for glucocorticoids in sensitizing the initial inflammatory response by the innate immune system.
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Glucocorticoid administration causes neutrophilia by expanding circulating neutrophils through increased bone marrow egress and hindered transmigration to inflammatory sites.
“Another salient outcome of GCs administration is neutrophilia. The steroid hormone expands the number of circulating neutrophils by (1) increasing their egress from the bone-marrow to the bloodstream and by (2) concomitantly hindering their transmigration to inflammatory sites by alleviating the expression of cell adhesion molecules (43, 44).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [43]
Combined exposure of human and murine myeloid cells to dexamethasone and ATP following LPS enhances the production of IL-1beta, TNF-alpha, IL-6, and IL-10.
“In fact, the combined exposure of human and murine myeloid cells to dexamethasone and ATP following LPS was found to enhance the production of IL-1β, TNF-α, IL-6, and IL-10 (43).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [43]
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- Authors
- Busillo, J. M., Azzam, K. M., & Cidlowski, J. A.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Cidlowski, John A.
- ORCID
- Cidlowski, John A.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 286
- Issue
- 44
- Pages
- 38703-38713
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3207479
- OpenAlex
- W2109356273
- Cited by
- 264
- References
- 62
- Citations by year
- 2026: 19 · 2025: 20 · 2024: 25 · 2023: 18 · 2022: 21 · 2021: 19 · 2020: 23 · 2019: 17 · 2018: 19 · 2017: 15 · 2016: 17 · 2015: 15 · 2014: 14 · 2013: 15 · 2012: 7
- FWCI
- 4.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Environmental Health Sciences (ZIAES090057)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- glucocorticoids, NLRP3 inflammasome, NOD-like receptors, innate immunity, glucocorticoid receptor, extracellular ATP, IL-1β, TNF-α, interleukin-6, anti-inflammatory agents
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Adenosine Triphosphate, Animals, Bone Marrow Cells, Carrier Proteins, Glucocorticoids, Immunity, Innate, Inflammation, Macrophages, Mice, Inbred C57BL, Receptors, Glucocorticoid, Tumor Necrosis Factor-alpha, Interleukin-6, Mice, Interleukin-1beta
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