Neutrophil recruitment and intracellular vesicle transport: A short overview

Masgrau-Alsina, Sergi; Sperandio, Markus; Rohwedder, Ina

doi:10.1111/eci.13237

Cited by 5 publications

(3 citation statements)

References 47 publications

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“…Neutrophils are a subset of granulocytes critical to the detection and elimination of microbes and foreign bodies. Neutrophils circulate in a quiescent state until activated by cytokines and growth factors released from sentinel cells such as endothelial cells ( 77 , 78 ). Once activated, neutrophils degranulate, or release stored pro-inflammatory mediators and/or microbicidal proteins, from either: i. primary or azurophilic, ii.…”

Section: Lyst Activity In Specific Cell Typesmentioning

confidence: 99%

The lysosomal trafficking regulator “LYST”: an 80-year traffic jam

Turner,

Che,

Mirhaidari

et al. 2024

Front. Immunol.

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Lysosomes and lysosome related organelles (LROs) are dynamic organelles at the intersection of various pathways involved in maintaining cellular hemostasis and regulating cellular functions. Vesicle trafficking of lysosomes and LROs are critical to maintain their functions. The lysosomal trafficking regulator (LYST) is an elusive protein important for the regulation of membrane dynamics and intracellular trafficking of lysosomes and LROs. Mutations to the LYST gene result in Chédiak-Higashi syndrome, an autosomal recessive immunodeficiency characterized by defective granule exocytosis, cytotoxicity, etc. Despite eight decades passing since its initial discovery, a comprehensive understanding of LYST’s function in cellular biology remains unresolved. Accumulating evidence suggests that dysregulation of LYST function also manifests in other disease states. Here, we review the available literature to consolidate available scientific endeavors in relation to LYST and discuss its relevance for immunomodulatory therapies, regenerative medicine and cancer applications.

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Section: Lyst Activity In Specific Cell Typesmentioning

confidence: 99%

The lysosomal trafficking regulator “LYST”: an 80-year traffic jam

Turner,

Che,

Mirhaidari

et al. 2024

Front. Immunol.

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“…Neutrophil recruitment is considered a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration (Nicu and Loos, 2016) [more details were reviewed by Masgrau et al (Masgrau-Alsina et al, 2020)].…”

Section: Recruitment Of Neutrophilsmentioning

confidence: 99%

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

Jiang

Zhao

Shui

et al. 2021

Front. Cell. Infect. Microbiol.

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Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis, a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a “wall” between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

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“…Several endothelial cell molecules, such as intracellular adhesion molecules (ICAM-1), vascular cell adhesion molecules (VCAM-1), junctional adhesion molecules (JAMs), endothelial cell-selective adhesion molecule (ESAM), platelet endothelial cell adhesion molecule-1 (PECAM-1), poliovirus receptor (PVR), CD99 and CD99L2, support TEM in a sequential fashion (Masgrau-Alsina et al, 2020).…”

Section: Biological Interpretationmentioning

confidence: 99%