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Transcriptome Sequencing Data of Peripheral Blood Neutrophils in Multiple Sclerosis Patients and Healthy Volunteers

ABSTRACT: Multiple sclerosis (MS) is a chronic, inflammatory, and demyelinating disease of the central nervous system. To explore the transcriptomic characteristics of peripheral blood neutrophils during the acute phase of MS, we conducted transcriptome sequencing analysis. Peripheral blood neutrophils were isolated from 8 MS patients in the acute phase and 29 age- and sex-matched healthy volunteers using density gradient centrifugation. RNA was extracted and sequenced on the Illumina platform to identify differentially expressed genes (DEGs) and their associated pathways. Bioinformatic analyses revealed significant alterations in genes related to immune response, neutrophil degranulation, and intracellular signaling. These findings provide insights into the molecular mechanisms underlying MS pathology and offer potential biomarkers for diagnosis and therapeutic targets.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288904 | GEO | 2025/02/17

REPOSITORIES: GEO

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Project description:Rationale: The acute respiratory distress syndrome is refractory to pharmacological intervention. Inappropriate activation of alveolar neutrophils is believed to underpin this disease’s complex pathophysiology, yet these cells have been little studied. Objectives: To examine the functional and transcriptional profiles of patient blood and alveolar neutrophils compared to healthy volunteer cells, and define their sensitivity to phosphoinositide 3-kinase inhibition. Methods: Twenty three ventilated patients underwent bronchoalveolar lavage. Alveolar and blood neutrophil apoptosis, phagocytosis and adhesion molecules were quantified by flow cytometry, and oxidase responses by chemiluminescence. Cytokine and transcriptional profiling utilized multiplex and GeneChip arrays. Measurements and Main Results: Patient blood and alveolar neutrophils were distinct from healthy circulating cells, with increased CD11b and reduced CD62L expression, delayed apoptosis and constitutively primed oxidase responses. Incubating control cells with disease bronchoalveolar lavage recapitulated the aberrant functional phenotype and this could be reversed by phosphoinositide 3-kinase inhibitors. In contrast, the pro-survival phenotype of patient cells was recalcitrant to phosphoinositide 3-kinase inhibition. RNA transcriptomic analysis revealed modified immune, cytoskeletal and cell death pathways in patient cells, aligning closely to sepsis and burns data sets but not with phosphoinositide 3-kinase signatures. Conclusions: Acute respiratory distress syndrome blood and alveolar neutrophils display a distinct primed, pro-survival profile and transcriptional signature. The enhanced respiratory burst was phosphoinositide 3-kinase-dependent, but delayed apoptosis and the altered transcriptional profile were not. These unexpected findings cast doubt over the utility of phosphoinositide 3-kinase inhibition in acute respiratory distress syndrome and highlight the importance of evaluating novel therapeutic strategies in patient-derived cells.

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Transcriptome Sequencing Data of Peripheral Blood Neutrophils in Multiple Sclerosis Patients and Healthy Volunteers

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