Lysozyme
Lysozyme is a protein associated with innate host defense and bacteriolysis.
Lysozyme is a protein associated with innate host defense and bacteriolysis. In the supplied literature, it is examined as a host factor in the control of Staphylococcus aureus, as a protein component of biological and nanoparticle-associated environments, and as a marker of distinct immune-cell states. Lysozyme-related signals occur alongside inflammatory mediators and pathways including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin 18 (IL-18), CXCL8, myeloperoxidase, and the NLRP3 inflammasome.
Recent work also treats lysozyme as a model protein for studying aggregation, crystallization, dry-powder formulation, and fibril-based biomaterials. Its detection in tear-protein coronas on iron oxide nanoparticles and in PET nanoplastic coronas illustrates how lysozyme can participate in protein–surface interactions. Across the supplied publications, the main research themes are lysozyme amyloid fibril formation, lysozyme in cancer and infection, and neuroinflammation after traumatic brain injury.
Rebuilt from PubMed 10 Sept 2026 · no new papers today
Where the papers sit
8 papers study lysozyme directly. The themes below are drawn from those 8. 1 new direction follows.
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Protein Assembly and Stability : Protein aggregation and interfacial organization are characterized across lysozyme solutions, nanoparticle coronas, fibrils, and dry powders. Recurring goals are stability, dispersibility, and control of nanoscale assemblies rather than a single therapeutic endpoint. 4 papers · 50%
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Aging and Brain Injury : Aging-dependent microglial heterogeneity and NLRP3 inflammasome activation recur in traumatic brain injury, alongside poorer survival. The work is defining how age-linked innate immune states shape injury severity and treatment targets. 2 papers · 25%
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Others — Host Defense and Cancer : Staphylococcus aureus control in atopic dermatitis and nanoplastic-corona-driven immune evasion in lung adenocarcinoma are the two themes. No shared biological direction is apparent. 2 papers · 25%
Lysozyme fibrils become ultrasound-activated intracellular piezocatalytic agents
The protein-fibril model using nanoparticle-conjugated lysozyme fibrils found that lysozyme can serve as a targeted, intracellular piezoelectric material rather than solely as a soluble protein, antimicrobial factor, formulation substrate, or corona component. Under ultrasound, the enhanced piezoelectricity generated reactive oxygen species inside targeted cells and induced apoptosis, establishing lysozyme fibrils as a potential mechanically activated therapeutic platform. 42166372May
Recent Findings on Lysozyme
Studies portray lysozyme as a dynamically organizing protein whose assemblies and interfaces depend on solution, surface, and formulation conditions. In lysozyme-NaCl solutions, dynamic light scattering detected oligomeric-sized populations, mesoscopic particles, and larger aggregates during crystallization-related restructuring 42680908Sep. The samples that formed crystals differed in mesoscopic-particle dynamics, showing that no single DLS peak predicted crystallization 42680908Sep. Other studies link lysozyme structure to carbohydrate composition in dry powders, nanoparticle protein-corona formation, and engineered fibrils for intracellular sono-piezocatalysis 42314049Jun42360315Jun42166372May. Together, these findings move toward controlling lysozyme’s multiscale organization for crystallization, aerosol delivery, nano-bio interfaces, and therapeutic piezocatalysis.
Studies identify lysozyme as an immune regulator whose effects vary with the biological context rather than as a uniformly bactericidal molecule. In atopic dermatitis, lysozyme does not kill Staphylococcus aureus but inhibits its exotoxin and exoenzyme production, while lysozyme levels decline alongside bacterial abundance during dupilumab treatment 42578672Aug. In contrast, lysozyme enriched in pathogenic PET nanoplastic coronas undergoes conformational remodeling, engages Toll-like receptor 4, and promotes efferocytosis-driven immune evasion in lung adenocarcinoma 42307976Jun. These contrasting outcomes direct attention toward lysozyme-dependent signaling and protein-corona biology alongside its role in controlling Staphylococcus aureus-associated inflammation.
Studies of traumatic brain injury converge on an age-dependent microglial shift from a Lysozyme+/Lyz2+ neuroprotective state toward an NLRP3+ and Interleukin-1β (IL-1β)-linked proinflammatory state 42294901Jun41926211Apr. Multiomics analyses associate the aged response with enhanced glycolysis, a proinflammatory chromatin landscape, and ELF1-driven transcription 42294901Jun41926211Apr. Microglia-targeted NLRP3 or ELF1 perturbation improved survival or recovery in aged mouse models, while one study also validated the microglial dichotomy in human TBI tissue 42294901Jun41926211Apr. Both studies therefore support ELF1 and the NLRP3 inflammasome as therapeutic targets, with imeglimin reversing the microglial phenotype and improving outcomes in aged mice 42294901Jun41926211Apr.
Written from 8 PubMed abstracts, each one cited by PMID above. Published: 2026-09-03. Last written: 2026-09-04 by GPT. Drafted by language models from published abstracts; not medical advice.