Evidence map›Paper›PMID 20447075›Full record

ReviewClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2010

SP-D and regulation of the pulmonary innate immune system in allergic airway changes.

L R Forbes, A Haczku

Open access · greenAbstract readReview
In one paragraph

Review in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Inhaled ozone induces distinct alterations in pulmonary function in models of acute and episodic exposure in female mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  5. Collectins and Ficolins.Advances in experimental medicine and biology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Genetic Polymorphisms of SP-A, SP-B, and SP-D and Risk of Respiratory Distress Syndrome in Preterm Neonates.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  18. Article
  19. Maternal allergen exposure reprograms the developmental lung transcriptome in atopic and normoresponsive rat pups.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  20. Article
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

2 authors at 1 institution in 1 country.

L R ForbesDepartment of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
A Haczku
University of Pennsylvania · US

Funding

Mechanisms of social-stress enhanced allergic airway response in a mouse modelR01AI072197 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2010 to 2014
$2.0M
Regulation of Inflammation in Asthma by Fas LigandR01HL076646 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2005 to 2009
$1.8M
Surfactant-Protein Innate Immunity in an Asthma ModelR01AI055593 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2004 to 2008
$1.6M
Effects of ozone exposure on expression and function of surfactant protein DRC1ES018505 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2009 to 2010
$1.0M
Surfactant-Protein Innate Immunity in an Asthma ModelR21AI055593 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI HACZKU, ANGELA · 2003 to 2003
$308k
NHLBI NIH HHS R01 HL076646NHLBI NIH HHS R01HL076646NIAID NIH HHS R01 AI055593NIAID NIH HHS R01AI055593NIAID NIH HHS R01 AI072197NIAID NIH HHS R21 AI055593NIEHS NIH HHS RC1 ES018505NIEHS NIH HHS RC1ES018505
6 · The paper itself

Abstract

The airway mucosal surfaces are constantly exposed to inhaled particles that can be potentially toxic, infectious or allergenic and should elicit inflammatory changes. The proximal and distal air spaces, however, are normally infection and inflammation free due to a specialized interplay between cellular and molecular components of the pulmonary innate immune system. Surfactant protein D (SP-D) is an epithelial-cell-derived immune modulator that belongs to the small family of structurally related Ca(2+)-dependent C-type collagen-like lectins. While collectins can be detected in mucosal surfaces of various organs, SP-A and SP-D (the 'lung collectins') are constitutively expressed in the lung at high concentrations. Both proteins are considered important players of the pulmonary immune responses. Under normal conditions however, SP-A-/- mice display no pathological features in the lung. SP-D-/- mice, on the other hand, show chronic inflammatory alterations indicating a special importance of this molecule in regulating immune homeostasis and the function of the innate immune cells. Recent studies in our laboratory and others implied significant associations between changes in SP-D levels and the presence of airway inflammation both in animal models and patients raising a potential usefulness of this molecule as a disease biomarker. Research on wild-type and mutant recombinant molecules in vivo and in vitro showed that SP-D binds carbohydrates, lipids and nucleic acids with a broad spectrum specificity and initiates phagocytosis of inhaled pathogens as well as apoptotic cells. Investigations on gene-deficient and conditional over expressor mice in addition, provided evidence that SP-D directly modulates macrophage and dendritic cell function as well as T cell-dependent inflammatory events. Thus, SP-D has a unique, dual functional capacity to induce pathogen elimination on the one hand and control of pro-inflammatory mechanisms on the other, suggesting a potential suitability for therapeutic prevention and treatment of chronic airway inflammation without compromising the host defence function of the airways. This paper will review recent findings on the mechanisms of immune-protective function of SP-D in the lung.

Indexed as

Gene Expression RegulationAnimalsHumansImmunity, InnateLungMicePulmonary Surfactant-Associated Protein DRespiratory HypersensitivityPulmonary Surfactant-Associated Protein D

Identifiers

PMID20447075
PMCPMC8894660
OpenAlexW1521369939

What OpenQuestion holds

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LicenceTDM
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.