Identification of the Cellular Sensor That Stimulates the Inflammatory Response to Sterile Cell Death
Open accessAbstract
Cell death provokes a robust inflammatory response. We have previously shown that this response is dependent on IL-1α. In this study, we investigate the cellular mechanism used by a host to sense cell death, produce IL-1α and also the role of IL-1β in this response. In almost all cases examined, the IL-1 that stimulated the death-induced inflammatory response came from the host rather than the cell that was dying. In these situations, host bone marrow-derived cells were the key source of the IL-1α that was required for the inflammatory response. Conditional cellular depletion and reconstitution in CD11b promoter-driven diphtheria toxin receptor transgenic mice revealed that host macrophages played an essential role in the generation of the inflammatory response and were the source of the required IL-1α. In addition, we found a role for IL-1β in the death-induced inflammatory response and that this cytokine was generated by both bone marrow-derived and radioresistant host cells. The one exception to these findings was that when dendritic cells were injected into mice, they provided a portion of the IL-1 that stimulated inflammation, and this was observed whether the dendritic cells were live or necrotic. Together, these findings demonstrate that macrophages play a key role as the primary sentinels that are required to sense and report cell death in ways that initiate the inflammatory response. One key way they accomplish this important task is by producing IL-1α that is needed to initiate the inflammatory response.
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In the case of necrotic liver tissue, IL-1α and IL-1β derived from resident macrophages, but not the necrotic cells themselves, seem to have a crucial role in eliciting the neutrophilic response.
“In the case of necrotic liver tissue, IL-1α and IL-1β derived from resident macrophages, but not the necrotic cells themselves, seem to have a crucial role in eliciting the neutrophilic response41.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [41]
Necrotic dendritic cells, but not necrotic macrophages, heart cells or liver cells, rely on IL-1α to recruit neutrophils, at least in a peritonitis model.
“For example, necrotic dendritic cells, but not necrotic macrophages, heart cells or liver cells, rely on IL-1α to recruit neutrophils, at least in a peritonitis model41.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [41]
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- Authors
- Kono, H., Karmarkar, D., Iwakura, Y., & Rock, K. L.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Institute of Medical Science, The University of Tokyo (JP)
- Corresponding author
- Kono, Hajime
- Karmarkar, Dipti
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-04
- Volume
- 184
- Issue
- 8
- Pages
- 4470-4478
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3094104
- OpenAlex
- W1897480893
- Cited by
- 101
- References
- 54
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 4 · 2022: 5 · 2021: 6 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 7 · 2013: 15 · 2012: 14
- FWCI
- 6.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI078287)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 32520, P30DK032520)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- inflammation, IL-1α, IL-1β, macrophages, dendritic cells, bone marrow-derived cells, diphtheria toxin receptor, necrosis, innate immunity
- MeSH terms
- Animals, Bone Marrow Cells, Cell Line, Transformed, Dendritic Cells, Humans, Inflammation, Interleukin-1, Mice, Inbred C57BL, Mice, Transgenic, Necrosis, Radiation Chimera, Cell Death, Macrophages, Peritoneal, Mice, Knockout, Inflammation Mediators, Intercellular Signaling Peptides and Proteins, CD11b Antigen, Cell Line, Tumor, Mice, Interleukin-1alpha, Interleukin-1beta, Heparin-binding EGF-like Growth Factor
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