Abstract
The inflammasomes are intracellular protein complexes that play an important role in innate immune sensing. Activation of inflammasomes leads to activation of caspase-1 and maturation and secretion of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18. In certain myeloid cells, this activation can also lead to an inflammatory cell death (pyroptosis). Inflammasome sensor proteins have evolved to detect a range of microbial ligands and bacterial exotoxins either through direct interaction or by detection of host cell changes elicited by these effectors. Bacterial exotoxins activate the inflammasomes through diverse processes, including direct sensor cleavage, modulation of ion fluxes through plasma membrane pore formation, and perturbation of various host cell functions. In this review, we summarize the findings on some of the bacterial exotoxins that activate the inflammasomes.
Highlights
Inflammasomes are multiprotein complexes that form in response to microbial effectors, metabolites, nucleic acids, and other danger signals
Monocytes were demonstrated to have a modest increase in cAMP in response to the mutant toxins, and monocytes pre-incubated with the toxins and co-cultured with CD4+ T cells led to an increase in IL-17A production in a caspase-1, IL-1β-dependent manner [101]
The recognition of self from non-self is the foundation of the innate immune response
Summary
The inflammasomes are intracellular protein complexes that play an important role in innate immune sensing. Activation of inflammasomes leads to activation of caspase-1 and maturation and secretion of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18. This activation can lead to an inflammatory cell death (pyroptosis). Inflammasome sensor proteins have evolved to detect a range of microbial ligands and bacterial exotoxins either through direct interaction or by detection of host cell changes elicited by these effectors. Bacterial exotoxins activate the inflammasomes through diverse processes, including direct sensor cleavage, modulation of ion fluxes through plasma membrane pore formation, and perturbation of various host cell functions. We summarize the findings on some of the bacterial exotoxins that activate the inflammasomes
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