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: 3 complete abstracts (571 words), 9 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
The tubular and cavernous organs and structures, by means of which pulmonary ventilation and gas exchange between ambient air and the blood are brought about.
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: Respiratory Systems; System, Respiratory; Respiratory Tract; Respiratory Tracts; Tract, Respiratory.
Where it fits in the MeSH classification
Research landscape
PubMed indexes 576,185 records tagged with the MeSH heading “Respiratory System” (counts retrieved 2026-10-31). 90,219 of them (15.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 266,040 records.
Reviews account for 45,084 records (7.8%) and meta-analyses for 1,922. Randomized controlled trials number 9,802 (1.7%) 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 | 266,040 |
| 2000-2009 | 94,383 |
| 2010-2019 | 125,543 |
| 2020 onward | 90,219 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 45,084 | 7.8% |
| Meta-analyses | 1,922 | 0.3% |
| Randomized controlled trials | 9,802 | 1.7% |
Method: PubMed query "Respiratory System"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Direct Numerical Simulations of Inhalation in a 23-Generation Lung Model | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42630053 · DOI · PMC13498875 |
| Niche exclusion of a lung pathogen in mice with designed probiotic communities | 2026 | Research article Design not recorded in structured metadata | 2 | cc0 PMID 42550883 · DOI · PMC13436956 |
| The airway epithelial-immune axis: mechanisms and therapeutic implications | 2026 | Review article Design not recorded in structured metadata | 2 | cc by PMID 42568577 · DOI · PMC13447427 |
Direct Numerical Simulations of Inhalation in a 23-Generation Lung Model [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The air flows in the proximal and distal portions of the human lungs are interconnected: the lower Reynolds number in the deeper generations causes a progressive flow regularization, but mass conservation requires flow rate oscillations to propagate through the airway bifurcations.
- Closing excerpt
- Even though these fluctuations are observed here in an idealized, rigid lung model, our findings suggest that the assumptions usually adopted in many of the current lung models might need to be revised.
- 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 (247 words)
The air flows in the proximal and distal portions of the human lungs are interconnected: the lower Reynolds number in the deeper generations causes a progressive flow regularization, but mass conservation requires flow rate oscillations to propagate through the airway bifurcations. To explain how these competing effects shape the flow state in the deeper generations, we have performed the first high-fidelity numerical simulation of the air flow in a lung model that includes 23 successive bifurcations of a single planar airway. Turbulence modeling or assumptions on flow regimes are not required. The chosen flow rate is steady on average, and representative of the peak inspiratory flow reached by adult patients breathing through therapeutic inhalers. As expected, advection becomes progressively less important after each bifurcation, until a time-dependent Stokes regime governed solely by viscous diffusion is established in the smallest generations. However, fluctuations in this regime are relatively fast and large with respect to the mean flow, which is in contrast with the commonly agreed picture that only the breathing frequency is relevant at the scale of the alveoli. We demonstrate that the characteristic frequency and amplitude of these fluctuations are linked to the flow in the upper part of the bronchial tree, as they originate from the time-dependent flow splitting in the upper bifurcations. Even though these fluctuations are observed here in an idealized, rigid lung model, our findings suggest that the assumptions usually adopted in many of the current lung models might need to be revised.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42630053 · DOI · PMC13498875
Niche exclusion of a lung pathogen in mice with designed probiotic communities [2]
Abstract reading summary — source excerpts
- Opening excerpt
- For years, the airway microbiota have been theorized to be gatekeepers of respiratory health, as pathogens entering the airway make contact with resident microbes prior to or coincident with their interaction with host cells.
- Closing excerpt
- This work serves as a foundation for the rational design of probiotic communities for protection against and treatment of respiratory infections.
- 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 (144 words)
For years, the airway microbiota have been theorized to be gatekeepers of respiratory health, as pathogens entering the airway make contact with resident microbes prior to or coincident with their interaction with host cells. Thus, modification of the native airway community may serve as a means of altering the local environment in favor of health. In this work, we hypothesize that synthetic bacterial communities introduced into the airway can serve as prophylactic countermeasures against infection by Burkholderia thailandensis in mice. We demonstrate that understanding of antagonistic interactions between a pathogen and airway microbiota in vitro can guide identification of probiotics with protective capabilities in vivo. Specifically, we show that niche overlap between the probiotic and pathogen is indicative of probiotic performance in vivo. This work serves as a foundation for the rational design of probiotic communities for protection against and treatment of respiratory infections.
Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 42550883 · DOI · PMC13436956
The airway epithelial-immune axis: mechanisms and therapeutic implications [3]
Abstract reading summary — source excerpts
- Opening excerpt
- The airway epithelium is increasingly recognized not merely as a physical barrier, but as a central, active regulator of mucosal immunity.
- Closing excerpt
- Furthermore, we highlight how emerging technologies-such as single-cell RNA sequencing, spatial transcriptomics, organoid models, and multi-omics integration-are decoding cellular heterogeneity and spatial niches, ultimately paving the way for precision medicine and long-term disease-modifying therapies in respiratory medicine.
- 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 (180 words)
The airway epithelium is increasingly recognized not merely as a physical barrier, but as a central, active regulator of mucosal immunity. This review comprehensively summarizes the structural and functional basis of the airway epithelial-immune axis and its critical role in chronic respiratory diseases. Exposure to environmental allergens, pollutants, and respiratory pathogens disrupts epithelial tight junctions and triggers the rapid release of key alarmins, including TSLP, IL-33, and IL-25. These epithelial-derived cytokines participate in reciprocal epithelial-immune circuits, driving extensive crosstalk with both innate (ILC2s) and adaptive (Th2 cells) immune networks to establish self-perpetuating inflammatory loops. Such epithelial dysfunction can act as an important driver and amplifier in the pathogenesis of asthma, chronic obstructive pulmonary disease (COPD), and upper airway inflammatory disorders. Consequently, targeting this axis has emerged as a promising therapeutic strategy, shifting the focus toward alarmin-neutralizing biologics, upstream receptor inhibition, and barrier restoration. Furthermore, we highlight how emerging technologies-such as single-cell RNA sequencing, spatial transcriptomics, organoid models, and multi-omics integration-are decoding cellular heterogeneity and spatial niches, ultimately paving the way for precision medicine and long-term disease-modifying therapies in respiratory medicine.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42568577 · DOI · PMC13447427
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 Respiratory function in patients post-infection by COVID-19: a systematic review and meta-analysis [4]
- Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [5]
- Research article Systematic review with meta-analysis of the accuracy of diagnostic tests for COVID-19 [6]
- Research article ACE2 Expression Is Increased in the Lungs of Patients With Comorbidities Associated With Severe COVID-19 [7]
- Research article Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk [8]
- Research article Pneumothorax rates in CT-Guided lung biopsies: a comprehensive systematic review and meta-analysis of risk factors [9]
References
- Atzori M, Gallorini E, Cottini C, Benassi A, Quadrio M. Direct Numerical Simulations of Inhalation in a 23-Generation Lung Model. . 2026. PMID 42630053 · DOI · PMC13498875
- Hern KE, Phillips AM, Mageeney CM, Williams KP, Sinha A, Carlson HK, et al.. Niche exclusion of a lung pathogen in mice with designed probiotic communities. . 2026. PMID 42550883 · DOI · PMC13436956
- Zhu Z, Li Q, Hua B. The airway epithelial-immune axis: mechanisms and therapeutic implications. . 2026. PMID 42568577 · DOI · PMC13447427
- Torres-Castro R, Vasconcello-Castillo L, Alsina-Restoy X, Solis-Navarro L, Burgos F, Puppo H, et al.. Respiratory function in patients post-infection by COVID-19: a systematic review and meta-analysis. Pulmonology. 2021. PMID 33262076 · DOI · PMC7687368
- McGoldrick E, Stewart F, Parker R, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2020. PMID 33368142 · DOI · PMC8094626
- Böger B, Fachi MM, Vilhena RO, Cobre AF, Tonin FS, Pontarolo R. Systematic review with meta-analysis of the accuracy of diagnostic tests for COVID-19. Am J Infect Control. 2021. PMID 32659413 · DOI · PMC7350782
- Pinto BGG, Oliveira AER, Singh Y, Jimenez L, Gonçalves ANA, Ogava RLT, et al.. ACE2 Expression Is Increased in the Lungs of Patients With Comorbidities Associated With Severe COVID-19. J Infect Dis. 2020. PMID 32526012 · DOI · PMC7377288
- Shrine N, Izquierdo AG, Chen J, Packer R, Hall RJ, Guyatt AL, et al.. Multi-ancestry genome-wide association analyses improve resolution of genes and pathways influencing lung function and chronic obstructive pulmonary disease risk. Nat Genet. 2023. PMID 36914875 · DOI · PMC10011137
- Huo YR, Chan MV, Habib AR, Lui I, Ridley L. Pneumothorax rates in CT-Guided lung biopsies: a comprehensive systematic review and meta-analysis of risk factors. Br J Radiol. 2020. PMID 31860329 · DOI · PMC7362905
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 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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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.