Mitogen-activated protein kinase phosphatase-1 controls PD-L1 expression by regulating type I interferon during systemic Escherichia coli infection

Barley, Timothy J.; Murphy, Parker R.; Wang, Xiantao; Bowman, Bridget; Mormol, Justin M.; Mager, Carli E; Kirk, Sean G.; Cash, Charles J.; Meng, Xiaomei; Nelin, Leif D.; Chen, Bernadette; Hafner, Markus; Zhang, Jian; Liu, Yusen

doi:10.1016/j.jbc.2022.101938

Cited by 2 publications

(1 citation statement)

References 66 publications

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“…Then macrophages are activated to secrete inflammation-related cytokines such as interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), and chemokines such as C–C motif chemokine 2 (CCL2) and CCL5 to recruit more macrophages and neutrophils to eliminate invasive microorganisms (Murray, 2017 ). CD86 and CD80 are also expressed in M1-polarized macrophages as surface markers, and iNOS (also called NO synthase 2, NOS2) is upregulated to synthesize more NO, which is an important messenger and effector molecule in the defense system of macrophages (Jungi et al, 1997 ; Barley et al, 2022 ). These factors potently contribute to the establishment of a pro-inflammatory activation state, which is commonly referred to as classical M1 macrophage activation (Bhatnagar et al, 2007 ; Hui et al, 2018 ).…”

Section: Mechanism Of Macrophage Polarizationmentioning

confidence: 99%

Extracellular vesicle-mediated regulation of macrophage polarization in bacterial infections

Zhu

Zhang

2022

Front. Microbiol.

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Extracellular vesicles (EVs) are nanoscale membrane-enveloped vesicles secreted by prokaryotic and eukaryotic cells, which are commonly defined as membrane vesicles (MVs) and exosomes, respectively. They play critical roles in the bacteria–bacteria and bacteria–host interactions. In infectious diseases caused by bacteria, as the first line of defense against pathogens, the macrophage polarization mode commonly determines the success or failure of the host's response to pathogen aggression. M1-type macrophages secrete pro-inflammatory factors that support microbicidal activity, while alternative M2-type macrophages secrete anti-inflammatory factors that perform an antimicrobial immune response but partially allow pathogens to replicate and survive intracellularly. Membrane vesicles (MVs) released from bacteria as a distinctive secretion system can carry various components, including bacterial effectors, nucleic acids, or lipids to modulate macrophage polarization in host–pathogen interaction. Similar to MVs, bacteria-infected macrophages can secrete exosomes containing a variety of components to manipulate the phenotypic polarization of “bystander” macrophages nearby or long distance to differentiate into type M1 or M2 to regulate the course of inflammation. Exosomes can also repair tissue damage associated with the infection by upregulating the levels of anti-inflammatory factors, downregulating the pro-inflammatory factors, and regulating cellular biological behaviors. The study of the mechanisms by which EVs modulate macrophage polarization has opened new frontiers in delineating the molecular machinery involved in bacterial pathogenesis and challenges in providing new strategies for diagnosis and therapy.

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Section: Mechanism Of Macrophage Polarizationmentioning

confidence: 99%

Extracellular vesicle-mediated regulation of macrophage polarization in bacterial infections

Zhu

Zhang

2022

Front. Microbiol.

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The implication of targeting PD-1:PD-L1 pathway in treating sepsis through immunostimulatory and anti-inflammatory pathways

Chen,

Guo,

Zhu

et al. 2023

Front. Immunol.

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Sepsis currently remains a major contributor to mortality in the intensive care unit (ICU), with 48.9 million cases reported globally and a mortality rate of 22.5% in 2017, accounting for almost 20% of all-cause mortality worldwide. This highlights the urgent need to improve the understanding and treatment of this condition. Sepsis is now recognized as a dysregulation of the host immune response to infection, characterized by an excessive inflammatory response and immune paralysis. This dysregulation leads to secondary infections, multiple organ dysfunction syndrome (MODS), and ultimately death. PD-L1, a co-inhibitory molecule expressed in immune cells, has emerged as a critical factor in sepsis. Numerous studies have found a significant association between the expression of PD-1/PD-L1 and sepsis, with a particular focus on PD-L1 expressed on neutrophils recently. This review explores the role of PD-1/PD-L1 in immunostimulatory and anti-inflammatory pathways, illustrates the intricate link between PD-1/PD-L1 and sepsis, and summarizes current therapeutic approaches against PD-1/PD-L1 in the treatment and prognosis of sepsis in preclinical and clinical studies.

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Mitogen-activated protein kinase phosphatase-1 controls PD-L1 expression by regulating type I interferon during systemic Escherichia coli infection

Cited by 2 publications

References 66 publications

Extracellular vesicle-mediated regulation of macrophage polarization in bacterial infections

Extracellular vesicle-mediated regulation of macrophage polarization in bacterial infections

The implication of targeting PD-1:PD-L1 pathway in treating sepsis through immunostimulatory and anti-inflammatory pathways

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