Ca2+-calmodulin signalling at the host-pathogen interface

Joseph J. Wanford; Charlotte Odendall

doi:10.1016/j.mib.2023.102267

Ca²⁺-calmodulin signalling at the host-pathogen interface

Joseph J. Wanford, Charlotte Odendall

Infectious Diseases

Research output: Contribution to journal › Review article › peer-review

7 Citations (Scopus)

Abstract

Multiple eukaryotic cell processes are modulated by calcium ions (Ca²⁺). As such, Ca²⁺ is emerging as a crucial regulator of innate immunity in multicellular organisms. In particular, recent studies have identified roles of Ca²⁺ signalling at the host-bacteria interface. Following microbial exposure, Ca²⁺ signals mobilised from the extracellular milieu or intracellular stores are transduced into cell physiological responses. However, during infection with host-adapted pathogens, Ca²⁺ signals are often atypical, due to the activities of virulence factors, with varied consequences for both the pathogen and the host cell. In this review, we describe the Ca²⁺-dependent host factors regulating antibacterial immunity, in addition to bacterial effectors that promote, inhibit, or co-opt Ca²⁺-calmodulin signalling to promote infection.

Original language	English
Article number	102267
Journal	Current Opinion in Microbiology
Volume	72
DOIs	https://doi.org/10.1016/j.mib.2023.102267
Publication status	Published - Apr 2023

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title = "Ca2+-calmodulin signalling at the host-pathogen interface",

abstract = "Multiple eukaryotic cell processes are modulated by calcium ions (Ca2+). As such, Ca2+ is emerging as a crucial regulator of innate immunity in multicellular organisms. In particular, recent studies have identified roles of Ca2+ signalling at the host-bacteria interface. Following microbial exposure, Ca2+ signals mobilised from the extracellular milieu or intracellular stores are transduced into cell physiological responses. However, during infection with host-adapted pathogens, Ca2+ signals are often atypical, due to the activities of virulence factors, with varied consequences for both the pathogen and the host cell. In this review, we describe the Ca2+-dependent host factors regulating antibacterial immunity, in addition to bacterial effectors that promote, inhibit, or co-opt Ca2+-calmodulin signalling to promote infection.",

author = "Wanford, {Joseph J.} and Charlotte Odendall",

note = "Funding Information: C. O. is supported by a Sir Henry Dale Fellowship from the Royal Society and the Wellcome Trust ( 206200/Z/17/Z ). For the purpose of open access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. Figures were created in Biorender. Publisher Copyright: {\textcopyright} 2023 The Authors",

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AU - Wanford, Joseph J.

AU - Odendall, Charlotte

N1 - Funding Information: C. O. is supported by a Sir Henry Dale Fellowship from the Royal Society and the Wellcome Trust ( 206200/Z/17/Z ). For the purpose of open access, the author has applied a CC BY public copyright licence to any Author Accepted Manuscript version arising from this submission. Figures were created in Biorender. Publisher Copyright: © 2023 The Authors

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N2 - Multiple eukaryotic cell processes are modulated by calcium ions (Ca2+). As such, Ca2+ is emerging as a crucial regulator of innate immunity in multicellular organisms. In particular, recent studies have identified roles of Ca2+ signalling at the host-bacteria interface. Following microbial exposure, Ca2+ signals mobilised from the extracellular milieu or intracellular stores are transduced into cell physiological responses. However, during infection with host-adapted pathogens, Ca2+ signals are often atypical, due to the activities of virulence factors, with varied consequences for both the pathogen and the host cell. In this review, we describe the Ca2+-dependent host factors regulating antibacterial immunity, in addition to bacterial effectors that promote, inhibit, or co-opt Ca2+-calmodulin signalling to promote infection.

AB - Multiple eukaryotic cell processes are modulated by calcium ions (Ca2+). As such, Ca2+ is emerging as a crucial regulator of innate immunity in multicellular organisms. In particular, recent studies have identified roles of Ca2+ signalling at the host-bacteria interface. Following microbial exposure, Ca2+ signals mobilised from the extracellular milieu or intracellular stores are transduced into cell physiological responses. However, during infection with host-adapted pathogens, Ca2+ signals are often atypical, due to the activities of virulence factors, with varied consequences for both the pathogen and the host cell. In this review, we describe the Ca2+-dependent host factors regulating antibacterial immunity, in addition to bacterial effectors that promote, inhibit, or co-opt Ca2+-calmodulin signalling to promote infection.

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Ca²⁺-calmodulin signalling at the host-pathogen interface

Abstract

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