ArticleJournal of inflammation research2026
Transforming Growth Factor-β1 Drives Neutrophil Chemokinesis, Not Chemotaxis.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Idiopathic pulmonary fibrosis (IPF) is a devastating condition that is characterized by dysregulated repair responses to alveolar epithelial damage and progressive remodeling of the lung interstitium. Neutrophils are critical responders to tissue injury, but their role in organ fibrosis pathogenesis remains unclear. Neutrophil numbers are increased in bronchoalveolar spaces of IPF patients, and neutrophil activation markers are elevated in fibrotic lung tissue. However, the key mediators driving neutrophil movement in fibrotic lung diseases are unknown. Transforming growth factor-beta 1 (TGFβ1) is a critical pro-fibrotic cytokine, but its effect on neutrophil movement remains unclear. This mechanistic, exploratory study aimed to determine whether TGFβ1 alters neutrophil migration in a direction-dependent (chemotaxis) or direction-independent (chemokinesis) manner and to assess whether TGFβ1 exposure is accompanied by functional changes consistent with neutrophil priming. Methods: This study utilized human neutrophils from healthy donors to model aspects of a TGFβ1-rich environment. Neutrophil movement was assessed using a transwell migration assay and by real-time tracking of human neutrophils within an Insall chamber. Extracellular release of superoxide anions and nucleic acid were assessed by lucigenin-amplified chemiluminescence, and fluorometry, respectively. Expression of cell surface markers, TGFβ receptor 1 and pSmad2/3 were assessed using flow cytometry and Western blot. Results: This study revealed that TGFβ1 drives neutrophil chemokinesis, but not chemotaxis, and that pre-treatment with TGFβ1 amplified selected movement responses to the established chemoattractants, interleukin-8 and N-Formylmethionine-leucyl-phenylalanine. TGFβ1 also increased total superoxide anion production and nucleic acid release, but did not alter cell surface expression of adhesion (CD11b and CD62L) or degranulation (CD66b) markers. Conclusion: Together, these data suggest that TGFβ1 promotes neutrophil chemokinesis, rather than chemotaxis, and that this may reflect transition into a priming-like state with potential relevance to neutrophil behavior in conditions such as fibrotic lung disease.
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