Targeting Interleukins Series: Interleukin-1 in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (20 February 2023) | Viewed by 3014

Special Issue Editor

Biological Sciences Department, The University of Texas at Dallas, 800 West Campbell Road, FO-1, Richardson, TX 75080, USA
Interests: inflammation; cancer; IL-1

Special Issue Information

Dear Colleagues,

The interleukin-1 (IL-1) family includes 11 cytokines and 10 receptors, where IL-1a, IL-1b, IL-1Ra, and their receptor, IL-1R1, are the most well characterized. As part of the healthy host defense, IL-1 mediates the innate immune response against tissue infection and injury caused by chemical and environmental stimuli or microbes. Damage-associated molecular pattern (DAMP) and pathogen-associated molecular pattern (PAMP) signaling caused by injury and infection, respectively, lead to IL-1 gene transcription, proteolytic cleavage, and activation. IL-1 signaling at the infection site recruits and/or activates immune, epithelial, endothelial, and fibroblast cells to facilitate tissue clearance of microbes and damaged cells and mediate tissue repair.  However, mutations or polymorphism in IL-1 or IL-1 regulators or chronic injury or infection lead to elevated or chronic IL-1 signaling that underlies inflammatory, autoimmune, malignant, and metabolic diseases. For example, normal IL-1 functions, including reactive oxygen production or the induction of VEGF secretion, are exploited by malignant cells in an inflammatory tumor microenvironment to promote disease progression. The role of IL-1 in disease is broad and complex, leading to the need for the development of multiple different IL-1 inhibitors that directly target IL-1 cytokines, IL-1 receptors, or IL-1 regulators. FDA-approved and investigational IL-1 inhibitors have been effective at alleviating symptoms of IL-1-triggered disease, emphasizing the culpability of IL-1 in disease initiation and progression.

This Special Edition on IL-1 in health and disease will report on the latest investigations into the mechanisms of IL-1 pathology and the latest (pre)clinical studies on the efficacy of IL-1 inhibitors in human disease.

Dr. Nikki Delk
Guest Editor

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Keywords

  • interleukin-1
  • IL-1
  • human disease
  • inflammation

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Published Papers (1 paper)

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Research

11 pages, 970 KiB  
Communication
Change in Eosinophil Count in Patients with Heart Failure Treated with Anakinra
by Michele Golino, Francesco Moroni, Marco Giuseppe Del Buono, Justin M. Canada, Azita H. Talasaz, Sebastian Piñel, James Mbualungu, Alessandra Vecchiè, Ai-Chen (Jane) Ho, Georgia K. Thomas, Salvatore Carbone, Hayley E. Billingsley, Jeremy Turlington, Roshanak Markley, Cory Trankle, Roberto De Ponti, Benjamin Van Tassell and Antonio Abbate
Cells 2023, 12(8), 1129; https://doi.org/10.3390/cells12081129 - 11 Apr 2023
Cited by 1 | Viewed by 2651
Abstract
Background: Interleukin-1 blockade with anakinra leads to a transient increase in eosinophil blood count (eosinophils) in patients with acute myocardial infarction. We aimed to investigate the effect of anakinra on changes in eosinophils in patients with heart failure (HF) and their correlation with [...] Read more.
Background: Interleukin-1 blockade with anakinra leads to a transient increase in eosinophil blood count (eosinophils) in patients with acute myocardial infarction. We aimed to investigate the effect of anakinra on changes in eosinophils in patients with heart failure (HF) and their correlation with cardiorespiratory fitness (CRF). Methods: We measured eosinophils in 64 patients with HF (50% females), 55 (51–63) years of age, before and after treatment, and, in a subset of 41 patients, also after treatment cessation. We also evaluated CRF, measuring peak oxygen consumption (VO2) with a treadmill test. Results: Treatment with anakinra significantly and transiently increased eosinophils, from 0.2 [0.1–0.3] to 0.3 [0.1–0.4] × 103 cells/µL (p < 0.001) and from 0.3 [0.2–0.5] to 0.2 [0.1–0.3] × 103 cells/µL, with suspension (p < 0.001). Changes in eosinophils correlated with the changes in peak VO2 (Spearman’s Rho = +0.228, p = 0.020). Eosinophils were higher in patients with injection site reactions (ISR) (n = 8, 13%; 0.5 [0.4–0.6] vs. 0.2 [0.1–0.4] × 103 cells/µL, p = 0.023), who also showed a greater increase in peak VO2 (3.0 [0.9–4.3] vs. 0.3 [−0.6–1.8] mLO2·kg−1·min−1, p = 0.015). Conclusion: Patients with HF treated with anakinra experience a transient increase in eosinophils, which is associated with ISR and a greater improvement in peak VO2. Full article
(This article belongs to the Special Issue Targeting Interleukins Series: Interleukin-1 in Health and Disease)
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