Macrophage Activation and Regulation

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

Deadline for manuscript submissions: 31 October 2024 | Viewed by 1135

Special Issue Editor


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Guest Editor
Faculty of Life Sciences & Medicine, King's College London, London, UK
Interests: macrophage; immunology; innate immunity; human induced pluripotent stem cells

Special Issue Information

Dear Colleagues,

Activated macrophages are a critical component of host defence that provides frontline protection against pathogens and malignant cells; they are also a potent inducer and a key regulator of inflammation. Dysregulated macrophage activation contributes to a spectrum of diseases ranging from immunodeficiency inflammatory/immune-mediated to degenerative diseases. George Mackaness first coined the term “macrophage activation” to describe a state of enhanced microbicidal capacity in response to antigen-non-specific stimuli. Since then, the concept has continually evolved through multiple revisions and refinements. Nathan et al. showed that interferon-gamma is the key inducer of “classical activation”, soon followed by Gordon et al.’s discovery that IL-4/13 induces an alternative activation. Mantovani proposed the M1/M2 paradigm; a more flexible spectrum model is now preferred by many investigators, avoiding binary definitions. More recently, Netea et al. championed the concept of “trained immunity” as an antigen-non-specific innate immune memory.

Over the years, much has been learned about the pathways that induce or regulate macrophage activation and their role in homeostasis and diseases. This Special Issue of Cells aims to highlight the latest developments and cutting-edge research in this exciting and ever-evolving field of research. We invite submissions of original research articles and comprehensive reviews from investigators across the globe.

Dr. Subhankar Mukhopadhyay
Guest Editor

Manuscript Submission Information

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Keywords

  • macrophage activation
  • classical and alternative activation
  • M1 and M2 activation, inflammatory and regulatory cytokines
  • inflammatory and pro-resolution lipid mediators
  • immune activatory and inhibitory receptors
  • ITAM and ITIMs

Published Papers (1 paper)

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Research

17 pages, 2691 KiB  
Article
The BK Channel Limits the Pro-Inflammatory Activity of Macrophages
by Yihe Chen, Nikita Markov, Lea Gigon, Aref Hosseini, Shida Yousefi, Darko Stojkov and Hans-Uwe Simon
Cells 2024, 13(4), 322; https://doi.org/10.3390/cells13040322 - 9 Feb 2024
Viewed by 850
Abstract
Macrophages play a crucial role in the innate immune response, serving as key effector cells in the defense against pathogens. Although the role of the large-conductance voltage and calcium-activated potassium channel, also known as the KCa1.1 or BK channel, in regulating [...] Read more.
Macrophages play a crucial role in the innate immune response, serving as key effector cells in the defense against pathogens. Although the role of the large-conductance voltage and calcium-activated potassium channel, also known as the KCa1.1 or BK channel, in regulating neurotransmitter release and smooth muscle contraction is well known, its potential involvement in immune regulation remains unclear. We employed BK-knockout macrophages and noted that the absence of a BK channel promotes the polarization of macrophages towards a pro-inflammatory phenotype known as M1 macrophages. Specifically, the absence of the BK channel resulted in a significant increase in the secretion of the pro-inflammatory cytokine IL-6 and enhanced the activity of extracellular signal-regulated kinases 1 and 2 (Erk1/2 kinases), Ca2+/calmodulin-dependent protein kinase II (CaMKII), and the transcription factor ATF-1 within M1 macrophages. Additionally, the lack of the BK channel promoted the activation of the AIM2 inflammasome without affecting the activation of the NLRC4 and NLRP3 inflammasomes. To further investigate the role of the BK channel in regulating AIM2 inflammasome activation, we utilized BK channel inhibitors, such as paxilline and iberiotoxin, along with the BK channel activator NS-11021. Pharmacological inactivation of the BK channel increased, and its stimulation inhibited IL-1β production following AIM2 inflammasome activation in wild-type macrophages. Moreover, wild-type macrophages displayed increased calcium influx when activated with the AIM2 inflammasome, whereas BK-knockout macrophages did not due to the impaired extracellular calcium influx upon activation. Furthermore, under conditions of a calcium-free medium, IL-1β production following AIM2 inflammasome activation was increased in both wild-type and BK-knockout macrophages. This suggests that the BK channel is required for the influx of extracellular calcium in macrophages, thus limiting AIM2 inflammasome activation. In summary, our study reveals a regulatory role of the BK channel in macrophages under inflammatory conditions. Full article
(This article belongs to the Special Issue Macrophage Activation and Regulation)
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