ArticleAnesthesia and analgesia2026
Protective and Immunomodulatory Functions of Exogenous B Cells in Experimental Hyperoxic Lung Injury.
Article in Anesthesia and analgesia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
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12 authors.
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Abstract
backgroundAcute respiratory distress syndrome (ARDS) is a result of diffuse lung injury and dysregulated inflammation. Recent studies have demonstrated that B cells can perform anti-inflammatory and tissue-protective functions. We hypothesized that systemic B-cell administration could have therapeutic effects in hyperoxic acute lung injury.
methodsAcute lung injury was modeled in adult C57BL/6J male mice through continuous exposure to hyperoxia (FiO 2 >90%). Mature B cells (CD45R + /CD19 + ) were purified from spleens of age- and sex-matched C57BL/6J mice. B cells (10 7 ) or saline were administered intravenously after 24 hours of hyperoxia. Hyperoxia exposure was continued for up to 96 hours. The effects of adoptive B-cell therapy were assessed using histologic, physiologic (pulse oximetry, echocardiography), and immunologic (flow cytometry) readouts.
resultsHyperoxia led to a 50% depletion of endogenous pulmonary B cells by day 3, from 30% to 15% CD45 + lung immune cells (95% confidence interval [CI], 6.16-24.45; P = .0017). B-cell administration ameliorated B-cell loss, improved lung injury scores (median score in saline-treated = 3.0 vs B-cell-treated = 2.67; P = .0101) and lung cellular infiltration (F [2,34] = 11.99; P = .0001). By day 3, B cells limited the duration of oxygen desaturations (difference 0.39 seconds; median length = 1.01 seconds in saline-treated vs 0.62 seconds in B-cell-treated; 95% CI, 0.02-0.73 seconds; P = .03) and their depth (median nadir = 82.0% in saline-treated vs 85.9% in B-cell-treated, 95% CI, -6.6% to -0.84%; P = .04). B-cell-treated mice showed a median 3.82% increase in left ventricular ejection fraction by day 3, compared to 12.35% in saline-treated mice (mean difference 7.32%; 95% CI, -5.0% to 19.6%; P = .23). Exogenous B cells represented less than 1.5% of pulmonary B cells on day 3. B-cell administration had homeostatic effects on relative abundance of pulmonary immune subsets affected by hyperoxia, including endogenous B cells, CD4 + T cells, natural killer (NK) cells, monocytes/macrophages, and neutrophils. Significant immunomodulatory effects of B-cell administration were observed in myeloid cells in the lungs and included reductions in the proportion of interleukin-17 (IL-17)-expressing Ly6C lo monocytes (F [2,14] = 19.02; P = .0001), alveolar macrophages (F [2,14] = 10.32; P = .0018), and neutrophils (F [2,14] = 6.621; P = .0095) as well as interferon-gamma (IFNγ)-expressing Ly6C lo monocytes (F [2,14] = 48.83; P = .0001).
conclusionsOur data indicate that adoptive B-cell therapy ameliorates hyperoxic lung injury and may represent a novel treatment for ARDS.
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