Evidence map›Paper›PMID 15742242›Full record

ReviewLung2004

Innate host defense of the lung: effects of lung-lining fluid pH.

Amelia W Ng, Akhil Bidani, Thomas A Heming

Abstract readReview
PubMed Publisher
In one paragraph

Review in Lung, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Exhaled Breath Analysis in Diagnosis of Malignant Pleural Mesothelioma: Systematic Review.International journal of environmental research and public health · 2020
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Respiratory Delivery ofPharmaceutics · 2024
    Article
  8. First Insight into the Degradome ofInternational journal of molecular sciences · 2024
    Article
  9. New approach methodologies (NAMs) for theFrontiers in toxicology · 2024
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. OvercomingOpen forum infectious diseases · 2022
    Review
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Amelia W NgDivision of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA.
Akhil Bidani
Thomas A Heming
The University of Texas Health Science Center at Houston · US

Funding

ALVEOLAR MACROPHAGE PHI REGULATION AND CELL FUNCTIONR01HL051421 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BIDANI, AKHIL · 1995 to 2003
$1.3M
NHLBI NIH HHS HL51421
6 · The paper itself

Abstract

Lung-lining fluid (LLF) is a primary constituent of the pulmonary host defense system. It is distributed continuously throughout the respiratory tract but is heterogeneous regarding its chemistry and physiology between the conducting airways and alveoli. The conducting airways are lined with airway surface liquid (ASL), a mucus gel-aqueous sol complex that interacts functionally with epithelial cilia as the mucociliary escalator. The alveoli are lined with alveolar subphase fluid (AVSF) and pulmonary surfactant. AVSF sterility is maintained in part by the phagocytic activity of resident alveolar macrophages. Normal ASL and AVSF are both more acidic than blood plasma. However, the details of acid-base regulation differ between the two media. Appreciable transepithelial acid-base flux is possible across the airway epithelium, whereas the alveolar epithelium is relatively impermeable to transepithelial acid-base flux. Moreover, one must consider the influence of resident macrophages on AVSF pH. Resident macrophages occupy a sizable fraction of AVSF by volume and are a substantial source of metabolic H+. The buffering capacities of ASL and AVSF probably are largely due to secreted peptides (e.g., ASL mucins and AVSF surfactant proteins). Acid-base exchange between the extracellular hydrophase and intracellular buffering systems of resident macrophages represents an additional buffer pool for AVSF. The pH of ASL and AVSF can be depressed by disease or inflammation. Low pH is predicted to suppress microbe clearance from the airways and alveoli, increase pathogen survival in both regions, and alter mediator release by resident macrophages and recruited leukocytes thereby increasing the propensity for bystander cell injury. Overall, ASL/AVSF pH is expected to be a major determinant of lung host defense responses.

Indexed as

Acid-Base EquilibriumBronchoalveolar Lavage FluidHumansHydrogen-Ion ConcentrationImmunity, InnateMacrophages, AlveolarPulmonary AlveoliRespiratory MucosaRespiratory Tract Diseases

Identifiers

PMID15742242
OpenAlexW2089925944

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.