Editorial: The role of glycolipids and sphingolipids in the differentiation and function of innate immune cells

Recent immunology research highlights the essential roles of glycolipids and sphingolipids in directing the differentiation and functions of innate immune cells, including macrophages, neutrophils, and innate T cells. These lipids support pathogen recognition, while many microorganisms exploit their own glycolipids to evade host defenses; for example, Mycobacterium Severe sepsis frequently progresses to acute respiratory distress syndrome (ARDS), where lung injury is driven by systemic inflammation and the release of neutrophil extracellular traps (NETs).While platelet-mediated NETosis is well established, the specific role of endothelial cells (ECs) has remained unclear, despite their significant dysfunction during sepsis. Fang et al. address this gap by demonstrating that the physical adhesion of neutrophils to ECs is a direct trigger for NET formation.They found that neutrophils firmly adherent to ECs-or ICAM-1-coated surfaces-rapidly generated NETs in response to inflammatory stimuli like LPS or septic plasma. Crucially, blocking the integrin Mac-1 disrupted this process both in vitro and in vivo, thereby attenuating LPS-induced lung injury.Study of stroke-associated pneumonia (SAP) is currently limited by animal models that lack the multisystem complexity-spanning neurological, pulmonary, and mucosal immune phenotypesobserved clinically. Here, Wang et al. introduce two rat models of SAP following intracerebral hemorrhage, utilizing either Klebsiella pneumoniae or lipopolysaccharide (LPS) challenge. These models demonstrated severe neurological deficits and tissue damage alongside intestinal dysfunction and a loss of IL-17A+ γδ T cells. In the Klebsiella cohort, 16S rRNA sequencing and metabolomics identified a shift toward opportunistic pathogens and aberrant metabolism, marked by elevated ceramide and quinolinic acid. These findings establish a critical tool for identifying therapeutic targets involving gut microbes. This issue highlights the impact of glycolipids and sphingolipids, whether originating from host leukocytes or pathogens, on cellular differentiation and immune function.. By deciphering these lipid interactions, we gain a clearer picture of innate immunity that can ultimately guide new treatment 5 strategies. 95 96

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Journal
Frontiers in Immunology
Published
2025-12-22
DOI
https://doi.org/10.3389/fimmu.2025.1758633
Primary Topic
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Type
article
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article

Editorial: The role of glycolipids and sphingolipids in the differentiation and function of innate immune cells

Kohji Kasahara, Kazuhisa Iwabuchi, Moriya Tsuji
Frontiers in Immunology
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
article

Editorial: The role of glycolipids and sphingolipids in the differentiation and function of innate immune cells

Kohji Kasahara, Kazuhisa Iwabuchi, Moriya Tsuji
article en

Abstract

Recent immunology research highlights the essential roles of glycolipids and sphingolipids in directing the differentiation and functions of innate immune cells, including macrophages, neutrophils, and innate T cells. These lipids support pathogen recognition, while many microorganisms exploit their own glycolipids to evade host defenses; for example, Mycobacterium Severe sepsis frequently progresses to acute respiratory distress syndrome (ARDS), where lung injury is driven by systemic inflammation and the release of neutrophil extracellular traps (NETs).While platelet-mediated NETosis is well established, the specific role of endothelial cells (ECs) has remained unclear, despite their significant dysfunction during sepsis. Fang et al. address this gap by demonstrating that the physical adhesion of neutrophils to ECs is a direct trigger for NET formation.They found that neutrophils firmly adherent to ECs-or ICAM-1-coated surfaces-rapidly generated NETs in response to inflammatory stimuli like LPS or septic plasma. Crucially, blocking the integrin Mac-1 disrupted this process both in vitro and in vivo, thereby attenuating LPS-induced lung injury.Study of stroke-associated pneumonia (SAP) is currently limited by animal models that lack the multisystem complexity-spanning neurological, pulmonary, and mucosal immune phenotypesobserved clinically. Here, Wang et al. introduce two rat models of SAP following intracerebral hemorrhage, utilizing either Klebsiella pneumoniae or lipopolysaccharide (LPS) challenge. These models demonstrated severe neurological deficits and tissue damage alongside intestinal dysfunction and a loss of IL-17A+ γδ T cells. In the Klebsiella cohort, 16S rRNA sequencing and metabolomics identified a shift toward opportunistic pathogens and aberrant metabolism, marked by elevated ceramide and quinolinic acid. These findings establish a critical tool for identifying therapeutic targets involving gut microbes. This issue highlights the impact of glycolipids and sphingolipids, whether originating from host leukocytes or pathogens, on cellular differentiation and immune function.. By deciphering these lipid interactions, we gain a clearer picture of innate immunity that can ultimately guide new treatment 5 strategies. 95 96

Frontiers in ImmunologyVol. 16
Aaron Diamond AIDS Research Center (US), Juntendo University (JP), Tokyo Metropolitan Institute of Medical Science (JP), Juntendo University Urayasu Hospital (JP)
Good health and well-being
Openalex Percentile: Top 37%
Neutrophil, Myeloperoxidase and Oxidative Mechanisms
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