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Togbe, D.

Publications and source records attributed to Togbe, D..

2 recordsLinked to original sources

Extracellular Vesicle-Enriched Secretome from Mesenchymal Stromal Cells Protects Against Chemically, Particulate-, and Ischemia-Induced Innate-Immunity Induced Inflammation

Mesenchymal stromal cells (MSCs) are multipotent cells with well-established regenerative and immunomodulatory properties, making them promising candidates for the treatment of inflammatory diseases. However, the therapeutic effects of MSCs are largely mediated by their secretome, particularly extracellular vesicles (EVs), which deliver bioactive molecules capable of modulating inflammatory responses. We generated an extracellular vesicle-enriched secretome (EVES) from MSCs under scalable, Good Manufacturing Practice (GMP)-compliant conditions and assessed its therapeutic efficacy in diverse disease models, including lung inflammation and kidney injury induced by distinct innate immune stimuli. EVES was isolated from the secretome of umbilical cord blood-derived MSCs cultured in a chemically defined medium. In vitro, EVES significantly and dose-dependently attenuated cytokine release from airway epithelial cells and macrophages stimulated with inflammatory agents such as lipopolysaccharide or reactive particles. In murine models of lung inflammation, EVES reduced neutrophil infiltration and suppressed multiple cytokines and chemokines in a dose-dependent manner. In models of kidney injury, EVES enhanced tubular epithelial cell proliferation, improved renal histology, and markedly reduced tubular necrosis following ischemia-reperfusion injury. Collectively, these findings demonstrate that MSC-derived EVES exhibits robust and broad-spectrum therapeutic activity across multiple disease contexts driven by innate immune activation, supporting its potential as a scalable, cell-free therapeutic platform.

cell biology↗

Hijacking of inflammasome responses by the complement system during Pseudomonas aeruginosa-Aspergillus fumigatus sur-infection

Patients with cystic fibrosis (pwCF) are highly susceptible to chronic pulmonary infections due to mutations in the CFTR gene. From early childhood, pwCF experience repeated lung infections and often develop chronic bacterial and/or fungal colonization. Among the most clinically relevant pathogens, Pseudomonas aeruginosa and Aspergillus fumigatus frequently co-infect and are associated with worse outcomes, including excessive IL-1{beta}-driven inflammation and accelerated lung function decline. Here we investigated the mechanisms underlying inflammasome overactivation during super-infection. We found that inflammasome hyperactivation occurred across macrophage populations, was independent of exogenous priming, and required live co-infection with both pathogens. P. aeruginosa and A. fumigatus cooperatively activated the NLRP3 inflammasome, and this response required both caspase-1 and caspase-8. Unexpectedly, gasdermin D was dispensable for IL-1{beta} release. Bacterial flagellin, type IV pili and the type III secretion system, as well as the fungal polysaccharide galactosaminogalactan (GAG), were each required for overactivation. Mechanistically, P. aeruginosa activated the MyD88-TLR pathway, enhancing macrophage responses and promoting ITGAM (CD11b) expression. Under fungal super-infection, macrophages secreted complement component C3, which may bound fungal surface and engaged the complement receptor C3R (CD11b/CD18). Downstream SYK and ERK signaling amplified inflammasome activation and IL-1{beta} release. Single-cell transcriptomic analysis of pwCF broncho-alveolar lavage and lung samples supported coordinated upregulation of complement and inflammasome pathways during bacterial-fungal infection. Together, these findings identify a complement-inflammasome signaling axis that drives pathological inflammation during bacterial-fungal co-infection in airways of pwCF and may represent a therapeutic target.

immunology↗