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Review
. 2021 May;20(3):2265-2285.
doi: 10.1111/1541-4337.12737. Epub 2021 Mar 26.

Pore-forming toxins of foodborne pathogens

Affiliations
Review

Pore-forming toxins of foodborne pathogens

Rajashri Banerji et al. Compr Rev Food Sci Food Saf. 2021 May.

Abstract

Pore-forming toxins (PFTs) are water-soluble molecules that have been identified as the most crucial virulence factors during bacterial pathogenesis. PFTs disrupt the host cell membrane to internalize or to deliver other bacterial or virulence factors for establishing infections. Disruption of the host cell membrane by PFTs can lead to uncontrollable exchanges between the extracellular and the intracellular matrix, thereby disturbing the cellular homeostasis. Recent studies have provided insights into the molecular mechanism of PFTs during pathogenesis. Evidence also suggests the activation of several signal transduction pathways in the host cell on recognition of PFTs. Additionally, numerous distinctive host defense mechanisms as well as membrane repair mechanisms have been reported; however, studies reveal that PFTs aid in host immune evasion of the bacteria through numerous pathways. PFTs have been primarily associated with foodborne pathogens. Infection and death from diseases by consuming contaminated food are a constant threat to public health worldwide, affecting socioeconomic development. Moreover, the emergence of new foodborne pathogens has led to the rise of bacterial antimicrobial resistance affecting the population. Hence, this review focuses on the role of PFTs secreted by foodborne pathogens. The review highlights the molecular mechanism of foodborne bacterial PFTs, assisting bacterial survival from the host immune responses and understanding the downstream mechanism in the activation of various signaling pathways in the host upon PFT recognition. PFT research is a remarkable and an important field for exploring novel and broad applications of antimicrobial compounds as therapeutics.

Keywords: bacterial toxins; food poisoning; foodborne diseases; pathogenesis; signaling cascade; virulence.

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References

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