Interplay between group A Streptococcus and host innate immune responses
MSW Su, YL Cheng, YS Lin, JJ Wu - Microbiology and Molecular …, 2024 - Am Soc Microbiol
MSW Su, YL Cheng, YS Lin, JJ Wu
Microbiology and Molecular Biology Reviews, 2024•Am Soc MicrobiolSUMMARY Group A Streptococcus (GAS), also known as Streptococcus pyogenes, is a
clinically well-adapted human pathogen that harbors rich virulence determinants
contributing to a broad spectrum of diseases. GAS is capable of invading epithelial,
endothelial, and professional phagocytic cells while evading host innate immune responses,
including phagocytosis, selective autophagy, light chain 3-associated phagocytosis, and
inflammation. However, without a more complete understanding of the different ways …
clinically well-adapted human pathogen that harbors rich virulence determinants
contributing to a broad spectrum of diseases. GAS is capable of invading epithelial,
endothelial, and professional phagocytic cells while evading host innate immune responses,
including phagocytosis, selective autophagy, light chain 3-associated phagocytosis, and
inflammation. However, without a more complete understanding of the different ways …
Summary
Group A Streptococcus (GAS), also known as Streptococcus pyogenes, is a clinically well-adapted human pathogen that harbors rich virulence determinants contributing to a broad spectrum of diseases. GAS is capable of invading epithelial, endothelial, and professional phagocytic cells while evading host innate immune responses, including phagocytosis, selective autophagy, light chain 3-associated phagocytosis, and inflammation. However, without a more complete understanding of the different ways invasive GAS infections develop, it is difficult to appreciate how GAS survives and multiplies in host cells that have interactive immune networks. This review article attempts to provide an overview of the behaviors and mechanisms that allow pathogenic GAS to invade cells, along with the strategies that host cells practice to constrain GAS infection. We highlight the counteractions taken by GAS to apply virulence factors such as streptolysin O, nicotinamide-adenine dinucleotidase, and streptococcal pyrogenic exotoxin B as a hindrance to host innate immune responses.
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