Dataset Information

Pathophysiological changes in plasma and BALF of patients with ARDS based on proteomics

ABSTRACT: Acute Respiratory Distress Syndrome (ARDS) remains a significant clinical challenge, with its pathogenesis not fully understood. Proteomic analyses of plasma and bronchoalveolar lavage fluid (BALF) in patients with ARDS have been performed to uncover diagnostic and prognostic markers, although previous studies have not adequately focused on longitudinal biomarker comparison. This study aims to elucidate the proteomic profiles of patients with ARDS in acute and subacute phases to better understand pathophysiological progression of ARDS.

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Plasma, Bronchoalveolar Lavage

DISEASE(S): Adult Respiratory Distress Syndrome

SUBMITTER: Fuminori Sugihara

LAB HEAD: Fuminori Sugihara

PROVIDER: PXD055757 | Pride | 2025-05-26

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	BALF01-40min_Slot2-1_1_20844.d.zip	Other
	BALF02-40min_Slot2-2_1_20846.d.zip	Other
	BALF03-40min_Slot2-3_1_20848.d.zip	Other
	BALF04-40min_Slot2-4_1_20850.d.zip	Other
	BALF06-40min_Slot2-6_1_20854.d.zip	Other

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Publications

Longitudinal proteomic analysis of pathophysiology in plasma and bronchoalveolar lavage fluid of patients with ARDS.

Mitsuyama Yumi Y Matsumoto Hisatake H Sugihara Fuminori F Fujimi Satoshi S Ogura Hiroshi H Oda Jun J

Journal of intensive care 20250515 1

<h4>Background</h4>Acute respiratory distress syndrome (ARDS) remains a significant clinical challenge, and its pathogenesis is not fully understood. Proteomic analyses of plasma and bronchoalveolar lavage fluid (BALF) in patients with ARDS have been performed to uncover diagnostic and prognostic markers, although previous studies have not adequately focused on longitudinal comparison of biomarkers. This study aimed to elucidate the proteomic profiles of patients with ARDS in the acute and subac ...[more]

PMID: 40375315

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Project description:SARS-CoV-2 is a novel coronavirus that causes acute respiratory distress syndrome (ARDS), death and long-term sequelae. Innate immune cells are critical for host defense but are also the primary drivers of ARDS. The relationships between innate cellular responses in ARDS resulting from COVID-19 compared to other causes of ARDS, such as bacterial sepsis is unclear. Moreover, the beneficial effects of dexamethasone therapy during severe COVID-19 remain speculative, but understanding the mechanistic effects could improve evidence-based therapeutic interventions. To interrogate these relationships, we developed an scRNAseq atlas that is freely accessible (biernaskielab.ca/COVID_neutrophil). We discovered that compared to bacterial ARDS, COVID-19 was associated with distinct neutrophil polarization characterized by either interferon (IFN) or prostaglandin (PG) active states. Neutrophils from bacterial ARDS had higher expression of antibacterial molecules such as PLAC8 and CD83. Dexamethasone therapy in COVID patients rapidly altered the IFNactive state, downregulated interferon responsive genes, and activated IL1R2+ve neutrophils. Dexamethasone also induced the emergence of immature neutrophils expressing immunosuppressive molecules ARG1 and ANXA1, which were not present in healthy controls. Moreover, dexamethasone remodeled global cellular interactions by changing neutrophils from information receivers into information providers. Importantly, male patients had higher proportions of IFNactive neutrophils and a greater degree of steroid-induced immature neutrophil expansion. Indeed, the highest proportion of IFNactive neutrophils was associated with mortality. These results define neutrophil states unique to COVID-19 when contextualized to other life-threatening infections, thereby enhancing the relevance of our findings at the bedside. Furthermore, the molecular benefits of dexamethasone therapy are also defined. The identified molecular pathways can now be targeted to develop improved therapeutics.