Exploring Periostin as a Biomarker in Asthma Research

Periostin, also described as osteoblast-specific factor-2 (OSF-2), is an extracellular matrix protein that is expressed in the periosteum. It plays an important role in normal tissue homeostasis and is highly expressed in pathological conditions in which trauma, inflammation, or tissue repair are involved (1). Periostin is therefore widely studied as a potential marker across several skeletal and non-skeletal diseases, including conditions related to lungs, asthma, allergy, liver, diabetes, kidney function, or cancer (2-5) .

In asthma, Periostin has also been implicated in several key aspects of allergic inflammation, including eosinophil recruitment, airway remodeling, promotion of a Th2-type immune response, and increased expression of inflammatory mediators (6-8).

Exploring Periostin as a Biomarker in Asthma Research

In a randomized trial researchers examined whether adults with stable T2-low asthma could safely reduce or discontinue inhaled corticosteroid treatment, while monitoring key biomarkers, including Periostin. Periostin was measured with the ELISA assay from Biomedica (9). 

Key takeaways:

• Asthma control remained stable over the 16-week dose-reduction period.
• Periostin levels increased when inhaled corticosteroid doses were reduced.
• Lowering the dose of inhaled corticosteroids may be feasible for some patients with stable T2-low asthma.
• Larger studies are needed to better understand which patients may benefit most.

 

Periostin can reliably be measured in biological fluids with a conventional ELISA assay

Periostin ELISA Highlights (Cat. No. BI-20433)

• Convenient – small sample volume – 10 µl / well
• Reliable  – full validation package
• Easy – 7 pre-diluted standards and 2 controls included
• Trusted – widely cited in +35 publications 
• Only assay that detects all known Periostin isoforms (citation no. 10)

 

Download our Periostin Flyer here

 

Tapering of inhaled corticosteroids in stable T2-low asthma: a randomized trial of symptom- and biomarker trajectories. Mosbech C et al., J Asthma. 2026; 63 (2), 206-213.

Abstract

Objective: To investigate whether tapering of inhaled corticosteroids (ICSs) is non-inferior to standard of care (SoC) in asthma patients with a stable type 2 (T2)-low inflammatory profile, generally considered less responsive to ICS therapy, and to describe symptom and biomarker trajectories during tapering.

Methods: This randomized, controlled, open-label multicenter trial conducted across specialist centers between 2022 and 2024 recruited adult asthma patients with persistently low T2 biomarkers, defined as blood eosinophils <0.15 × 10⁹/L, fractional exhaled nitric oxide (FeNO) <25 ppb, and non-allergic phenotype. Patients’ adherent to medium- or high-dose ICS were randomized 1:1 to either ICS tapering (50% reduction at randomization and withdrawal after 8 weeks) or continued SoC. The primary endpoint was change in Asthma Control Questionnaire (ACQ) score at 16 weeks. Secondary endpoints included changes in blood and sputum eosinophils, FeNO, periostin, and lung function.

Results: Recruitment proved challenging as only 20 of 2766 screened patients met eligibility criteria, leading to early study termination. Median ACQ remained stable in the tapering group (0 [-0.14; 0.5]) and improved modestly in the SoC group (-0.44 [-0.9; -0.11]; p = 0.211). FeNO (p = 0.038) and periostin (p = 0.031) increased with tapering but remained within the T2 low range. Minimal changes were observed in blood eosinophils (p = 0.3) and FEV₁ (p = 0.7).

Conclusions: Premature trial termination due to recruitment challenges reflects the rarity of stable T2-low asthma. ICS tapering was not associated with greater symptom deterioration compared to SoC, although non-inferiority was not demonstrated.

Literature:

1. Periostin in Osteoporosis and Cardiovascular Disease. Pickering ME, Oris C, Chapurlat R. J Endocr Soc. 2023; 6;7(7):bvad081. PMID: 37362382.
2. Periostin action in bone. Mol Cell Endocrinol. Bonnet N, Garnero P, Ferrari S.2016 ; 5;432:75-82. PMID: 26721738.
3. The role of periostin in lung fibrosis and airway remodeling. O’Dwyer DN, Moore BB. Cell Mol Life Sci. 2017; 74(23):4305-4314. PMID: 28918442.
4. Periostin in the Kidney. Wallace DP. Adv Exp Med Biol. 2019;1132:99-112.  PMID: 31037629.
5. Periostin: biology and function in cancer. Dorafshan S, Razmi M, Safaei S, Gentilin E, Madjd Z, Ghods R. Cancer Cell Int. 2022; 12;22(1):315. PMID: 36224629.
6. Roles of Periostin in Asthma. Matsumoto H. Adv Exp Med Biol. 2019;1132:145-159. PMID: 31037633.
7. Periostin: its role in asthma and its potential as a diagnostic or therapeutic target. Li W, Gao P, Zhi Y, Xu W, Wu Y, Yin J, Zhang J.Respir Res. 2015 May 17;16(1):57. doi: 10.1186/s12931-015-0218-2. PMID: 25981515; PMCID: PMC4437675.
8. Asthma Inflammatory Phenotypes: How Can We Distinguish Them? Plavsic A, Bonaci-Nikolic B, Milenkovic B, Miskovic R, Kusic N, Dimitrijevic M, Arandjelovic S, Milosevic K, Buha I, Tomic Spiric V. J Clin Med. 2024 Jan 17;13(2):526. doi: 10.3390/jcm13020526. PMID: 38256660; PMCID: PMC10816410.
9. Tapering of inhaled corticosteroids in stable T2-low asthma: a randomized trial of symptom- and biomarker trajectories. Mosbech, Godtfredsen, Christiansen, Bak, Ulrik, Westergaar. J Asthma. 2026; 63 (2), 206-213. PMID: 41160477.
10. Characterization of a sandwich ELISA for the quantification of all human periostin isoforms. Gadermaier, E., Tesarz, M., Suciu, A.A.-M., Wallwitz, J., Berg, G., Himmler, G., 2018. J. Clin. Lab. Anal. 32, e22252.PMID:28493527.