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Immune Evasion and Interaction Between Autophagy and Intracellular Staphylococcus aureus

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Staphylococcus aureus
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Abstract

Staphylococcus aureus found on human skin is an opportunistic pathogen that causes a variety of infections. Although this bacterium has been considered as an extracellular pathogen, several studies have demonstrated that S. aureus is able to internalize and replicate in both professional and non-professional phagocytic cells. This intracellular niche is important for escape from humoral immunity and antibiotics, and is relevant to recurrent and chronic infections of S. aureus. For intracellular survival, S. aureus develops mechanisms to resist the innate immune response, particularly a cellular homeostatic autophagy. Autophagy is thought to be a cellular defense system that transfers invading pathogens to lysosomes for elimination. Therefore, understanding the interaction between S. aureus and autophagy is important to prevent recurrent and chronic S. aureus infections. This chapter focuses on the interaction between S. aureus and autophagy to understand how this bacterium evades this innate immune degradation or combats autophagy for intracellular survival.

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Abbreviations

agr:

Accessary gene regulator

Atg5:

Autophagy-related protein 5

BRCA1:

Neighbor of breast cancer susceptibility gene 1

CALCOCO2:

Calcium binding and coiled-coil domain 2

cAMP:

Cyclic adenosine monophosphate

Hla:

Alpha hemolysin

LC3:

Microtubule-associated protein 1A/1B-light chain 3

MAPK 14:

Mitogen-activated protein kinase 14

PI3K:

Phosphoinositide-3-kinase

PMN:

Polymorphonuclear neutrophils

SCV:

Small colony variant

TSST-1:

Toxic shock syndrome toxin-1

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Asano, K. (2024). Immune Evasion and Interaction Between Autophagy and Intracellular Staphylococcus aureus. In: Nakane, A., Asano, K. (eds) Staphylococcus aureus. Springer, Singapore. https://doi.org/10.1007/978-981-99-9428-1_6

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