Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (784 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the bronchioles leading to an obstructive lung disease. Bronchioles are characterized by fibrous granulation tissue with bronchial exudates in the lumens. Clinical features include a nonproductive cough and dyspnea.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Bronchiolitis, Exudative; Bronchiolitides, Exudative; Exudative Bronchiolitides; Exudative Bronchiolitis; Bronchiolitis, Proliferative; Proliferative Bronchiolitis; Bronchiolitides, Proliferative; Proliferative Bronchiolitides.
Where it fits in the MeSH classification
- Broader topics
- Bronchiolitis
- Narrower topics
- Organizing Pneumonia
Related concepts
- Bronchioles
- Dyspnea
Research landscape
PubMed indexes 4,665 records tagged with the MeSH heading “Bronchiolitis Obliterans” (counts retrieved 2026-11-04). 889 of them (19.1%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,430 records.
Reviews account for 733 records (15.7%) and meta-analyses for 14. Randomized controlled trials number 54 (1.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,004 |
| 2000-2009 | 1,342 |
| 2010-2019 | 1,430 |
| 2020 onward | 889 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 733 | 15.7% |
| Meta-analyses | 14 | 0.3% |
| Randomized controlled trials | 54 | 1.2% |
Method: PubMed query "Bronchiolitis Obliterans"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in respiratory medicine
Research on airway and lung disease mixes lung-function tests, symptom diaries, imaging and hospital records, so what was measured and in whom matters as much as the result. Many conditions here, such as asthma and COPD, vary between people and over time, and exposure studies (smoking, pollution, workplace dust) show association rather than proof of cause. Nothing on this page is advice about treatment or inhalers; anyone with breathing difficulty should seek care from a qualified clinician. Check how the condition was defined, the severity of the people studied and whether outcomes were symptoms, lung function or hospital admissions.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Postinfectious Bronchiolitis Obliterans in Children: Diagnostic Workup and Therapeutic Options: A Workshop Report [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Bronchiolitis obliterans (BO) is a rare, chronic form of obstructive lung disease, often initiated with injury of the bronchiolar epithelium followed by an inflammatory response and progressive fibrosis of small airways resulting in nonuniform luminal obliteration or narrowing.
- Closing excerpt
- Since 2016, an international consortium of experts with an interest in PIBO assembles on a regular basis in Geisenheim, Germany, to discuss key areas in PIBO which include diagnostic workup, treatment strategies, and research fields.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (187 words)
Bronchiolitis obliterans (BO) is a rare, chronic form of obstructive lung disease, often initiated with injury of the bronchiolar epithelium followed by an inflammatory response and progressive fibrosis of small airways resulting in nonuniform luminal obliteration or narrowing. The term BO comprises a group of diseases with different underlying etiologies, courses, and characteristics. Among the better recognized inciting stimuli leading to BO are airway pathogens such as adenovirus and mycoplasma, which, in a small percentage of infected children, will result in progressive fixed airflow obstruction, an entity referred to as postinfectious bronchiolitis obliterans (PIBO). The present knowledge on BO in general is reasonably well developed, in part because of the relatively high incidence in patients who have undergone lung transplantation or bone marrow transplant recipients who have had graft-versus-host disease in the posttransplant period. The cellular and molecular pathways involved in PIBO, while assumed to be similar, have not been adequately elucidated. Since 2016, an international consortium of experts with an interest in PIBO assembles on a regular basis in Geisenheim, Germany, to discuss key areas in PIBO which include diagnostic workup, treatment strategies, and research fields.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32076469 · DOI · PMC7013295
Modulation of NLRP3 Inflammasome through Formyl Peptide Receptor 1 (Fpr-1) Pathway as a New Therapeutic Target in Bronchiolitis Obliterans Syndrome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Chronic rejection is the major leading cause of morbidity and mortality after lung transplantation.
- Closing excerpt
- We underline the importance of the NLRP3 inflammasome and the pathogenic role of Fpr-1 in experimental models of BOS, which is the result of the modulation of immune cell recruitment together with the modulation of local cellular activation, suggesting this gene as a new target in the control of the pathologic features of BOS.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (233 words)
Chronic rejection is the major leading cause of morbidity and mortality after lung transplantation. Bronchiolitis obliterans syndrome (BOS), a fibroproliferative disorder of the small airways, is the main manifestation of chronic lung allograft rejection. We investigated, using transgenic mice, the mechanisms through which the deficiency of IL-1β/IL-18, Casp-1, or Fpr-1 genes could be protective in an experimental model of BOS, induced in mice by allogeneic heterotopic tracheal transplantation. Fpr-1 KO mice showed a marked reduction in histological markers of BOS and of mast cell numbers compared to other groups. Molecular analyses indicated that the absence of the Fpr-1 gene was able to decrease NF-κB nuclear translocation and modulate NLRP3 inflammasome signaling and the mitogen-activated protein kinase (MAPK) pathway in a more significant way compared to other groups. Additionally, Fpr-1 gene deletion caused a reduction in resistance to the apoptosis, assessed by the TUNEL assay. Immunohistochemical analyses indicated changes in nitrotyrosine, PARP, VEGF, and TGF-β expression associated with the pathology, which were reduced in the absence of the Fpr1 gene more so than by the deletion of IL-1β/IL-18 and Casp-1. We underline the importance of the NLRP3 inflammasome and the pathogenic role of Fpr-1 in experimental models of BOS, which is the result of the modulation of immune cell recruitment together with the modulation of local cellular activation, suggesting this gene as a new target in the control of the pathologic features of BOS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32244997 · DOI · PMC7139667
Reprogramming alveolar macrophage responses to TGF-β reveals CCR2+ monocyte activity that promotes bronchiolitis obliterans syndrome [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Bronchiolitis obliterans syndrome (BOS) is a major impediment to lung transplant survival and is generally resistant to medical therapy.
- Closing excerpt
- Thus, through studying the effects of ECP, we have identified an AM functional plasticity that controls a TGF-β-dependent network that couples CCR2+ monocyte recruitment and differentiation to alloimmunity and BOS.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (182 words)
Bronchiolitis obliterans syndrome (BOS) is a major impediment to lung transplant survival and is generally resistant to medical therapy. Extracorporeal photophoresis (ECP) is an immunomodulatory therapy that shows promise in stabilizing BOS patients, but its mechanisms of action are unclear. In a mouse lung transplant model, we show that ECP blunts alloimmune responses and inhibits BOS through lowering airway TGF-β bioavailability without altering its expression. Surprisingly, ECP-treated leukocytes were primarily engulfed by alveolar macrophages (AMs), which were reprogrammed to become less responsive to TGF-β and reduce TGF-β bioavailability through secretion of the TGF-β antagonist decorin. In untreated recipients, high airway TGF-β activity stimulated AMs to express CCL2, leading to CCR2+ monocyte-driven BOS development. Moreover, we found TGF-β receptor 2-dependent differentiation of CCR2+ monocytes was required for the generation of monocyte-derived AMs, which in turn promoted BOS by expanding tissue-resident memory CD8+ T cells that inflicted airway injury through Blimp-1-mediated granzyme B expression. Thus, through studying the effects of ECP, we have identified an AM functional plasticity that controls a TGF-β-dependent network that couples CCR2+ monocyte recruitment and differentiation to alloimmunity and BOS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36189800 · DOI · PMC9525120
Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Bronchiolitis obliterans syndrome (BOS) is a progressive, fatal obstructive lung disease that occurs following lung transplant, where it is termed chronic lung allograft dysfunction BOS (CLAD-BOS), or as the primary manifestation of pulmonary chronic graft versus host disease (cGVHD-BOS) following allogeneic hematopoietic stem cell transplant.
- Closing excerpt
- These data suggest substantial cellular and molecular overlap between CLAD- and cGVHD-BOS and, therefore, common pathways for possible therapeutic intervention.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (182 words)
Bronchiolitis obliterans syndrome (BOS) is a progressive, fatal obstructive lung disease that occurs following lung transplant, where it is termed chronic lung allograft dysfunction BOS (CLAD-BOS), or as the primary manifestation of pulmonary chronic graft versus host disease (cGVHD-BOS) following allogeneic hematopoietic stem cell transplant. Disease pathogenesis is poorly understood; however, chronic alloreactivity is common to both conditions, suggesting a shared pathophysiology. We performed single-cell RNA-Seq (scRNA-Seq) on explanted human lungs from 4 patients with CLAD-BOS, 3 patients with cGVHD-BOS, and 3 deceased controls to identify cell types, genes, and pathways enriched in BOS to better understand disease mechanisms. In both forms of BOS, we found an expanded population of CD8+ tissue resident memory T cells (TRM), which was distinct to BOS compared with other chronic lung diseases. In addition, BOS samples expressed genes and pathways associated with macrophage chemotaxis and proliferation, including in nonimmune cell populations. We also identified dysfunctional stromal cells in BOS, characterized by pro- and antifibrotic gene programs. These data suggest substantial cellular and molecular overlap between CLAD- and cGVHD-BOS and, therefore, common pathways for possible therapeutic intervention.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40232854 · DOI · PMC12128974
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Bronchiolitis obliterans syndrome 2001: an update of the diagnostic criteria [5]
- Research article Cryptogenic organising pneumonia [6]
- Research article Obliterative bronchiolitis [7]
- Research article Bronchiolitis obliterans and other late onset non-infectious pulmonary complications in hematopoietic stem cell transplantation [8]
- Research article Organising pneumonia [9]
- Research article Post-transplant bronchiolitis obliterans [10]
References
- Jerkic SP, Brinkmann F, Calder A, Casey A, Dishop M, Griese M, et al.. Postinfectious Bronchiolitis Obliterans in Children: Diagnostic Workup and Therapeutic Options: A Workshop Report. . 2020. PMID 32076469 · DOI · PMC7013295
- D'Amico R, Fusco R, Cordaro M, Siracusa R, Peritore AF, Gugliandolo E, et al.. Modulation of NLRP3 Inflammasome through Formyl Peptide Receptor 1 (Fpr-1) Pathway as a New Therapeutic Target in Bronchiolitis Obliterans Syndrome. . 2020. PMID 32244997 · DOI · PMC7139667
- Liu Z, Liao F, Zhu J, Zhou D, Heo GS, Leuhmann HP, et al.. Reprogramming alveolar macrophage responses to TGF-β reveals CCR2+ monocyte activity that promotes bronchiolitis obliterans syndrome. . 2022. PMID 36189800 · DOI · PMC9525120
- Mellors PW, Lange AN, Casino Remondo B, Shestov M, Planer JD, Peterson AR, et al.. Shared roles of immune and stromal cells in the pathogenesis of human bronchiolitis obliterans syndrome. . 2025. PMID 40232854 · DOI · PMC12128974
- Estenne M, Maurer JR, Boehler A, Egan JJ, Frost A, Hertz M, et al.. Bronchiolitis obliterans syndrome 2001: an update of the diagnostic criteria. J Heart Lung Transplant. 2002. PMID 11897517 · DOI
- Cordier JF. Cryptogenic organising pneumonia. Eur Respir J. 2006. PMID 16880372 · DOI
- Barker AF, Bergeron A, Rom WN, Hertz MI. Obliterative bronchiolitis. N Engl J Med. 2014. PMID 24806161 · DOI
- Afessa B, Litzow MR, Tefferi A. Bronchiolitis obliterans and other late onset non-infectious pulmonary complications in hematopoietic stem cell transplantation. Bone Marrow Transplant. 2001. PMID 11593314 · DOI
- Cordier JF. Organising pneumonia. Thorax. 2000. PMID 10722773 · DOI · PMC1745738
- Boehler A, Estenne M. Post-transplant bronchiolitis obliterans. Eur Respir J. 2003. PMID 14680094 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.