{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T20:03:59Z","timestamp":1790193839392,"version":"4.1.0"},"reference-count":43,"publisher":"S. Karger AG","issue":"8","license":[{"start":{"date-parts":[[2021,1,1]],"date-time":"2021-01-01T00:00:00Z","timestamp":1609459200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2021,1,1]],"date-time":"2021-01-01T00:00:00Z","timestamp":1609459200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Respiration"],"published-print":{"date-parts":[[2021]]},"abstract":"<jats:p>&lt;b&gt;&lt;i&gt;Background:&lt;\/i&gt;&lt;\/b&gt; Emerging evidence has indicated that small airway dysfunction (SAD) contributes to the clinical expression of asthma. &lt;b&gt;&lt;i&gt;Objectives:&lt;\/i&gt;&lt;\/b&gt; The aim of the study was to explore the relationships of SAD assessed by forced expiratory flow between 25 and 75% (FEF&lt;sub&gt;25\u201375&lt;\/sub&gt;%), with clinical and inflammatory profile and treatment responsiveness in asthma. &lt;b&gt;&lt;i&gt;Method:&lt;\/i&gt;&lt;\/b&gt; In study I, dyspnea intensity (Borg scale), chest tightness, wheezing and cough (visual analog scales, VASs), and pre- and post-methacholine challenge testing (MCT) were analyzed in asthma patients with SAD and non-SAD. In study II, asthma subjects with SAD and non-SAD underwent sputum induction, and inflammatory mediators in sputum were detected. Asthma patients with SAD and non-SAD receiving fixed treatments were prospectively followed up for 4 weeks in study III. Spirometry, Asthma Control Questionnaire (ACQ), and Asthma Control Test (ACT) were carried out to define treatment responsiveness. &lt;b&gt;&lt;i&gt;Results:&lt;\/i&gt;&lt;\/b&gt; SAD subjects had more elevated \u0394VAS for dyspnea (&lt;i&gt;p&lt;\/i&gt; = 0.027) and chest tightness (&lt;i&gt;p&lt;\/i&gt; = 0.032) after MCT. Asthma patients with SAD had significantly elevated interferon (IFN)-\u03b3 in sputum (&lt;i&gt;p&lt;\/i&gt; &amp;#x3c; 0.05), and Spearman partial correlation found FEF&lt;sub&gt;25\u201375&lt;\/sub&gt;% significantly related to IFN-\u03b3 and interleukin-8 (both having &lt;i&gt;p&lt;\/i&gt; &amp;#x3c; 0.05). Furthermore, multivariable regression analysis indicated SAD was significantly associated with worse treatment responses (decrease in ACQ \u22650.5 and increase in ACT \u22653) (&lt;i&gt;p&lt;\/i&gt; = 0.022 and &lt;i&gt;p&lt;\/i&gt; = 0.032). &lt;b&gt;&lt;i&gt;Conclusions:&lt;\/i&gt;&lt;\/b&gt; This study indicates that SAD in asthma predisposes patients to greater dyspnea intensity and chest tightness during bronchoconstriction. SAD patients with asthma are characterized by non-type 2 inflammation that may account for poor responsiveness to therapy.<\/jats:p>","DOI":"10.1159\/000515328","type":"journal-article","created":{"date-parts":[[2021,4,23]],"date-time":"2021-04-23T17:04:34Z","timestamp":1619197474000},"page":"767-779","source":"Crossref","is-referenced-by-count":5,"title":["Small Airway Dysfunction in Asthma Is Associated with Perceived Respiratory Symptoms, Non-Type 2 Airway Inflammation, and Poor Responses to Therapy"],"prefix":"10.1159","volume":"100","author":[{"given":"Ying","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong Lin","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin 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