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 (635 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
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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: Lungs.
Where it fits in the MeSH classification
- Broader topics
- Respiratory System
- Narrower topics
- Bronchi; Pulmonary Alveoli
- See also
- Air Sacs; Pneumonectomy; Pulmonary Circulation; Respiration
Research landscape
PubMed indexes 329,633 records tagged with the MeSH heading “Lung” (counts retrieved 2026-10-31). 57,050 of them (17.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 155,130 records.
Reviews account for 26,398 records (8.0%) and meta-analyses for 976. Randomized controlled trials number 4,602 (1.4%) 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 | 155,130 |
| 2000-2009 | 49,412 |
| 2010-2019 | 68,041 |
| 2020 onward | 57,050 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 26,398 | 8.0% |
| Meta-analyses | 976 | 0.3% |
| Randomized controlled trials | 4,602 | 1.4% |
Method: PubMed query "Lung"[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 |
| Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 42373669 · DOI · PMC13458731 |
| The Gut-Lung Microbiome Crosstalk and Pulmonary Disease | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 42352300 · DOI · PMC13297202 |
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
Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Lung mononuclear phagocyte subsets differ in their ability to restrict Mycobacterium tuberculosis (Mtb) during chronic infection, yet the mechanisms underlying this difference are not well defined.
- Closing excerpt
- Overcoming or bypassing impaired IFNγ responsiveness may guide the development of more effective tuberculosis vaccines and host-directed therapies.
- 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 (148 words)
Lung mononuclear phagocyte subsets differ in their ability to restrict Mycobacterium tuberculosis (Mtb) during chronic infection, yet the mechanisms underlying this difference are not well defined. Here, we show that CD11clo monocyte-derived cells, the subset of lung cells that is most permissive for Mtb viability during chronic infection, express lower levels of interferon-gamma (IFNγ) signaling proteins, resulting in reduced responses to IFNγ compared to alveolar macrophages and CD11chi monocyte-derived cells. Moreover, type I IFN signaling suppresses IFNγ-mediated MHC class II expression, impairing antigen-specific CD4 T cell activation by CD11clo monocyte-derived cells. Importantly, prior immunity conferred by contained Mtb infection enhances IFNγ responsiveness of monocyte-derived cells, reducing bacterial burdens in lungs and within monocyte-derived cell subsets. Our findings indicate that heterogeneous IFNγ responsiveness is exploited by Mtb for persistence in vivo. Overcoming or bypassing impaired IFNγ responsiveness may guide the development of more effective tuberculosis vaccines and host-directed therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42373669 · DOI · PMC13458731
The Gut-Lung Microbiome Crosstalk and Pulmonary Disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Both the gut and the lungs possess a microbiome, a community of commensal bacteria, archaea, fungi, and viruses that perform important housekeeping functions in those organs.
- Closing excerpt
- Diet, tobacco smoking and electronic cigarette vaping all impact both the gut and lung microbiomes.
- 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 (240 words)
Both the gut and the lungs possess a microbiome, a community of commensal bacteria, archaea, fungi, and viruses that perform important housekeeping functions in those organs. The colonic microbiome primarily ferments indigestible dietary fibers into essential short-chain fatty acids, synthesizes essential vitamins, regulates the mucosal immune system, and forms a protective barrier against pathogenic colonization. The lung microbiome maintains respiratory health primarily by regulating mucosal immunity, providing a physical barrier against invading pathogens, and producing beneficial metabolites. Several colonic microbiota metabolites, including the short-chain fatty acids acetate, propionate, and butyrate, together with the tryptophan metabolites indole-3-acetate and indole-3-propionate, secondary bile acids, and the polyamines spermidine and putrescine, are transported to the lungs via the gut-lung axis. These colonic microbiota biomolecules suppress lung inflammation, strengthen immune homeostasis, and reduce the severity of respiratory diseases. In contrast, lung microorganisms and their metabolites can travel to the gut via the gut-lung axis, influencing intestinal immune responses and potentially leading to an imbalance of gut microorganisms or dysbiosis. This means that respiratory diseases may lead to digestive issues, intestinal inflammation and chronic diseases. Here, we have reviewed this crosstalk and its impact on the principal pulmonary diseases: asthma, chronic obstructive pulmonary disease, cystic fibrosis, bronchogenic carcinoma, COVID-19, interstitial lung diseases, pneumonia, and tuberculosis. It is concluded that the gut microbiome plays a significant part in lung health and disease. Diet, tobacco smoking and electronic cigarette vaping all impact both the gut and lung microbiomes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42352300 · DOI · PMC13297202
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 Radiation dose-volume effects in the lung [4]
- Research article Complication rates of CT-guided transthoracic lung biopsy: meta-analysis [5]
- Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [6]
- Research article New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries [7]
- Research article Respiratory function in patients post-infection by COVID-19: a systematic review and meta-analysis [8]
- Research article Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth [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
- Zheng W, Limberis JD, Howard ZP, Mohapatra A, Takagi E, Ernst JD. Impaired IFNγ responsiveness of monocyte-derived lung cells limits immunity to Mycobacterium tuberculosis. . 2026. PMID 42373669 · DOI · PMC13458731
- Beyoğlu D, Idle JR. The Gut-Lung Microbiome Crosstalk and Pulmonary Disease. . 2026. PMID 42352300 · DOI · PMC13297202
- Marks LB, Bentzen SM, Deasy JO, Kong FM, Bradley JD, Vogelius IS, et al.. Radiation dose-volume effects in the lung. Int J Radiat Oncol Biol Phys. 2010. PMID 20171521 · DOI · PMC3576042
- Heerink WJ, de Bock GH, de Jonge GJ, Groen HJ, Vliegenthart R, Oudkerk M. Complication rates of CT-guided transthoracic lung biopsy: meta-analysis. Eur Radiol. 2017. PMID 27108299 · DOI · PMC5127875
- Roberts D, Brown J, Medley N, Dalziel SR. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev. 2017. PMID 28321847 · DOI · PMC6464568
- Shrine N, Guyatt AL, Erzurumluoglu AM, Jackson VE, Hobbs BD, Melbourne CA, et al.. New genetic signals for lung function highlight pathways and chronic obstructive pulmonary disease associations across multiple ancestries. Nat Genet. 2019. PMID 30804560 · DOI · PMC6397078
- 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
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.