Special Issue "Macrophage Interplay with Pore-Forming Toxins"

A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 5525

Special Issue Editor

Dr. Peter A. Keyel
E-Mail Website
Guest Editor
Department of Biological Sciences, Texas Tech University, Box 43131 Lubbock, TX 79409, USA
Interests: cholesterol-dependent cytolysin; membrane repair; inflammasome; macrophage; Dnase1L3
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

One critical innate immune cell type is the macrophage. Macrophages play key roles in pathogen clearance and tissue repair. Many pathogens secrete pore-forming toxins (PFTs), which macrophages must detect, then defend against them and respond to them. Similarly, macrophages also detect and respond to innate immune PFTs deployed against bacteria, and target cells, including perforin and the membrane, attack the complex of complement. Finally, macrophages themselves utilize PFTs like gasdermin D and mixed-lineage kinase-like (mlkl) to execute the cell death pathways of pyroptosis and necroptosis, respectively, to deny intracellular pathogens refuge. Interplay between macrophages and toxins occurs at many steps and leaves many unknowns in the field. Three broad outstanding questions in the field are: How do macrophages discriminate between PFTs to correctly promote or suppress inflammation? What molecular mechanisms drive macrophage responses to PFTs? How do bacteria and other pathogens hijack macrophage responses to PFTs to promote infection?

This Special Issue will focus on the interplay between macrophages and related myeloid cells with pore-forming toxins, including both the use of pore-forming toxins by these cells, and the response of these cells to toxins. This includes the biology behind cell death processes that require pore-forming toxins, macrophage responses to external toxins deployed against other bacteria and cells, and inflammation, immunosuppression, signaling, and other responses to pore-forming toxins.

Asst. Prof. Dr. Peter A. Keyel
Guest Editor

Manuscript Submission Information

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Keywords

  • pore-forming toxin
  • pyroptosis
  • mlkl
  • inflammation
  • host–pathogen interaction
  • cell death

Published Papers (2 papers)

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Review

Review
Interaction of Macrophages and Cholesterol-Dependent Cytolysins: The Impact on Immune Response and Cellular Survival
Toxins 2020, 12(9), 531; https://doi.org/10.3390/toxins12090531 - 19 Aug 2020
Cited by 10 | Viewed by 2180
Abstract
Cholesterol-dependent cytolysins (CDCs) are key virulence factors involved in many lethal bacterial infections, including pneumonia, necrotizing soft tissue infections, bacterial meningitis, and miscarriage. Host responses to these diseases involve myeloid cells, especially macrophages. Macrophages use several systems to detect and respond to cholesterol-dependent [...] Read more.
Cholesterol-dependent cytolysins (CDCs) are key virulence factors involved in many lethal bacterial infections, including pneumonia, necrotizing soft tissue infections, bacterial meningitis, and miscarriage. Host responses to these diseases involve myeloid cells, especially macrophages. Macrophages use several systems to detect and respond to cholesterol-dependent cytolysins, including membrane repair, mitogen-activated protein (MAP) kinase signaling, phagocytosis, cytokine production, and activation of the adaptive immune system. However, CDCs also promote immune evasion by silencing and/or destroying myeloid cells. While there are many common themes between the various CDCs, each CDC also possesses specific features to optimally benefit the pathogen producing it. This review highlights host responses to CDC pathogenesis with a focus on macrophages. Due to their robust plasticity, macrophages play key roles in the outcome of bacterial infections. Understanding the unique features and differences within the common theme of CDCs bolsters new tools for research and therapy. Full article
(This article belongs to the Special Issue Macrophage Interplay with Pore-Forming Toxins)
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Review
The Dual Function of the Fungal Toxin Candidalysin during Candida albicans—Macrophage Interaction and Virulence
Toxins 2020, 12(8), 469; https://doi.org/10.3390/toxins12080469 - 24 Jul 2020
Cited by 6 | Viewed by 3015
Abstract
The dimorphic fungus Candida albicans is both a harmless commensal organism on mucosal surfaces and an opportunistic pathogen. Under certain predisposing conditions, the fungus can overgrow the mucosal microbiome and cause both superficial and life-threatening systemic infections after gaining access to the bloodstream. [...] Read more.
The dimorphic fungus Candida albicans is both a harmless commensal organism on mucosal surfaces and an opportunistic pathogen. Under certain predisposing conditions, the fungus can overgrow the mucosal microbiome and cause both superficial and life-threatening systemic infections after gaining access to the bloodstream. As the first line of defense of the innate immune response, infecting C. albicans cells face macrophages, which mediate the clearance of invading fungi by intracellular killing. However, the fungus has evolved sophisticated strategies to counteract macrophage antimicrobial activities and thus evade immune surveillance. The cytolytic peptide toxin, candidalysin, contributes to this fungal defense machinery by damaging immune cell membranes, providing an escape route from the hostile phagosome environment. Nevertheless, candidalysin also induces NLRP3 inflammasome activation, leading to an increased host-protective pro-inflammatory response in mononuclear phagocytes. Therefore, candidalysin facilitates immune evasion by acting as a classical virulence factor but also contributes to an antifungal immune response, serving as an avirulence factor. In this review, we discuss the role of candidalysin during C. albicans infections, focusing on its implications during C. albicans-macrophage interactions. Full article
(This article belongs to the Special Issue Macrophage Interplay with Pore-Forming Toxins)
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