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. 2025 Apr;80(4):1154-1157.
doi: 10.1111/all.16453. Epub 2024 Dec 21.

Oncostatin-M Is Produced by Human Eosinophils and Expression Is Increased in Uncontrolled Severe Asthma

Stephane Esnault  1   2 , Ksenija Bernau  2 , Heather L Floerke  2 , Arnaud Dendooven  1 , Emeline Delaunay  1 , Kimberly A Dill-McFarland  3 , Matthew C Altman  3   4 , William W Busse  2 , Melissa A Rosenkranz  5   6 , Matthew C Tattersall  7 , Mats W Johansson  2 , Julien Labreuche  8 , Delphine Beury  9 , Shéhérazade Sebda  9 , Frédéric Dezoteux  1   10   11 , Baptiste Segard  1   12 , Geoffrey Mortuaire  1   11   12 , Delphine Staumont-Sallé  1   10   11 , Thomas Stoup  1 , Cécile Chenivesse  11   13   14 , Nathan Sandbo  2 , Nizar N Jarjour  2 , Guillaume Lefèvre  1   11   15
Affiliations

Oncostatin-M Is Produced by Human Eosinophils and Expression Is Increased in Uncontrolled Severe Asthma

Stephane Esnault et al. Allergy. 2025 Apr.
No abstract available

Keywords: CRSwNP; Oncostatin M; allergy; asthma; bronchoalveolar lavage; cytolysis; degranulation; eosinophils; severe asthma.

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Conflict of interest statement

K. Bernau received funding from the Pulmonary Fibrosis Foundation, by an independent grant from Boehringer Ingelheim Pharmaceuticals Inc. who provided the financial support outside of the submitted work. W. W. Busse reports consulting fees/honoraria from GlaxoSmithKline, Regeneron, Sanofi, and Genentech, and royalties from Elsevier. N. N. Jarjour received research funding from AstraZeneca for extension of the National Institutes of Health–funded severe asthma research program; and received consulting fees over the past 3 years from GlaxoSmithKline, Chiese, and AstraZeneca related to asthma treatment. K. A. Dill‐McFarland reports consulting fees from Seattle BioSoftware and EuropaDX related to computational tool development. F. Dezoteux was investigator for clinical trials sponsored by Abbvie, Almirall, Amgen, AstraZeneca, Eli Lilly, Galderma, Leo Pharma, Novartis, Pfizer, and Sanofi‐Regeneron; received consulting fees by AbbVie, Almirall, Eli Lilly, Galderma, Leo Pharma, Novartis, Pfizer, Sanofi‐Regeneron, and UCB. D. Staumont‐Sallé received funding from AstraZeneca for a research study in DRESS syndrome; was investigator for clinical trials sponsored by Abbvie, Almirall, Amgen, AstraZeneca, Eli Lilly, Galderma, Leo Pharma, Novartis, Pfizer, and Sanofi‐Regeneron; received consulting fees by AbbVie, Almirall, AstraZeneca, Eli Lilly, Galderma, GSK, Leo Pharma, Novartis, Pfizer, Sanofi‐Regeneron, and UCB. C. Chenivesse declares research grants from AstraZeneca, GlaxoSmithKlein, Santelys, and Novartis, personal fees from ALK‐Abello, AstraZeneca, Boehringer Ingelheim, Chiesi, Sanofi, and GlaxoSmithKlein and congress support from AstraZeneca, Boehringer Ingelheim, Chiesi, and Novartis. G. Lefèvre received consulting fees, personal fees for advisory boards or meetings, and research fundings from AstraZeneca and GSK. These relationships with pharmaceutical companies are not relevant to the current study. M. W. Johansson received funding from Hoffmann‐La Roche, outside of the submitted work. The rest of the authors declare that they have no relevant conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Oncostatin‐M is expressed and released by eosinophils, and it is associated with airway eosinophilia and inflammatory mediators after SBP‐Ag. (A) (left panel) Blood eosinophils were activated with IL3 (2 ng/mL) for 20 h and then seeded on heat‐aggregated IgG (IL3IgG) or no IgG (IL3) for 6 h. Oncostatin‐M was quantified in eosinophil cultures by ELISA. (middle and right panel) Blood eosinophils from four healthy donors were activated with IL3 (10 ng/mL) or eotaxin‐1 (100 ng/mL) for 6 h. mRNA expression level was determined by 3′UTR RNA‐sequencing. Variance stabilizing transformations (VST) for CD69 and OSM are shown. Graphs present medians within 25th and 75th percentiles. *Adjusted p < 0.05 compared to Control. (B) BALF oncostatin‐M of 18 subjects before (D0) and after SBP‐Ag (D2) was quantified by ELISA. Change in BALF oncostatin‐M concentration correlated with change in number of BALF eosinophils. (C) Change in BALF oncostatin‐M post‐vs‐pre SBP‐Ag was analyzed for correlations with the change of the other detected BALF proteins using the inflammation panel from Olink technology. The 26 most correlated proteins with OSM are shown (FDR ≤ 0.01). (D) Linear fold changes in BALF oncostatin‐M correlated with changes in blood oncostatin‐M as measured in serum using Olink technology.
FIGURE 2
FIGURE 2
Expression level of OSM in blood eosinophils is increased in severe asthma and it is associated with ACQ and number of exacerbations. Isolated blood eosinophils from 19 healthy controls, 21 patients with severe asthma and 18 with chronic rhinosinusitis with polyps without asthma underwent RNA‐sequencing. (A) Participants' characteristics. (B) Isolated blood eosinophils underwent RNA‐sequencing and variance stabilizing transformation (VST) and adjustment for sex was applied to the fold changes in expression level between groups. Median OSM level and interquartile range with 75th and 25th percentile is shown. For differences of expression level of genes between asthma patients and the other groups, p values adjusted for multiple comparisons were determined for all genes using the FDR procedure (Benjamini–Hochberg) and were reported for OSM. (C) OSM levels in eosinophils from the patients with asthma were analyzed for correlations with ACQ and number (Nb) of exacerbations in the last 12 months (Pearson).
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References

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