Stress-induced interleukin-6 release in mice is mast cell-dependent and more pronounced in Apolipoprotein E knockout mice
Abstract
Objective Interleukin-6 (IL-6) is elevated in the serum of patients with coronary artery disease (CAD) and acute coronary syndromes (ACS). Intracoronary release of IL-6 was reported in ACS that can also be triggered by acute stress. In rats, acute restraint stress increases serum IL-6 and histamine, both of which may derive from mast cells. The current study was carried out in order to determine any possible difference in stress-induced IL-6 release in atherosclerotic mice and the contribution of mast cells, corticotropin-releasing hormone (CRH) and urocortin (Ucn). Methods C57BL/6J, W/W(v) mast cell-deficient, Apolipoprotein E (ApoE) and CRH knockout (k/o) mice were stressed in plexiglass restraint chambers for 15 to 120 min. Serum corticosterone and IL-6 levels were measured. Some C57BL and ApoE k/o mice were pretreated with either the mast cell stabilizer disodium cromoglycate (cromolyn) or the peptide CRH receptor (CRH-R) antagonist Astressin. Cardiac mast cell activation was studied in both C57BL and ApoE k/o mice using light microscopy. Results Acute stress increased serum IL-6 in mice, an effect much greater in ApoE k/o atherosclerotic mice. Stress-induced IL-6 release was absent in W/W(v) mast cell-deficient mice and it was partially inhibited by cromolyn in C57BL and ApoE mice. Mast cells were found adjacent to atherosclerotic vessels in ApoE k/o mice and were activated after stress. CRH k/o mice released more IL-6 in response to stress than their wild types, but Ast…
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The background IL-6 concentration in untreated mice was <10 pg/mL.
“The background IL-6 concentration in untreated mice was <10 pg/mL, which corresponds to previously reported values (Huang et al., 2003).”
From Model Based Targeting of IL-6-Induced Inflammatory Responses in Cultured Primary Hepatocytes to Improve Application of the JAK Inhibitor Ruxolitinib (2017) · cites this paper as Huang et al., 2003
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- Authors
- Huang, M.
- Affiliations
- Tufts University (US)
- Corresponding author
- Huang, M
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2003-07-01
- Volume
- 59
- Issue
- 1
- Pages
- 241-249
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W2075414471
- Cited by
- 96
- References
- 1
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 6 · 2023: 1 · 2022: 5 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 3 · 2017: 5 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 4 · 2012: 6
- FWCI
- 1.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- interleukin-6, acute stress, mast cells, ApoE-deficient mice, atherosclerosis, corticotropin-releasing factor, urocortin, restraint stress, coronary inflammation, acute coronary syndrome, disodium cromoglycate, astressin, corticosterone
- MeSH terms
- Animals, Apolipoproteins E, Coronary Disease, Corticosterone, Corticotropin-Releasing Hormone, Cromolyn Sodium, Mast Cells, Mice, Inbred C57BL, Peptide Fragments, Stress, Physiological, Interleukin-6, Receptors, Corticotropin-Releasing Hormone, Mice, Knockout, Mice, Urocortins
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