Surfactant alterations in severe pneumonia, acute respiratory distress syndrome, and cardiogenic lung edema
Abstract
Bronchoalveolar lavage fluids (BALF) were analyzed for surfactant abnormalities in 153 patients with acute respiratory failure necessitating mechanical ventilation. Diagnoses were acute respiratory distress syndrome (ARDS) in the absence of lung infection (n = 16), severe pneumonia (PNEU; n = 88), ARDS and PNEU (n = 36), and cardiogenic lung edema (CLE; n = 13). The PNEU group was subdivided into groups with alveolar PNEU (n = 35), bronchial PNEU (n = 16), interstitial PNEU (n = 18) and nonclassified PNEU (n = 19). Comparison with healthy controls (n = 20) was undertaken. Total phospholipids (PL), proteins, PL classes (HPTLC) and surfactant apoproteins SP-A and SP-B (ELISA) were quantified in the original BALF. The 48,000 x g pellet from centrifugation of the BAL was used to assess the percentage of large surfactant aggregates (LSA) and the biophysical properties of the surfactant (pulsating bubble surfactometer). All groups with inflammatory lung injury (PNEU and/or ARDS) showed some decrease in the lavageable PL pool, a reduced LSA content in BALF, and a manifold increase in alveolar protein load. Marked changes in the PL profile were noted throughout the groups (a decrease in phosphatidylcholine (PC) and phosphatidylglycerol (PG) and an increase in phosphatidylinositol [PI] and sphingomyelin [SPH]). Concentrations of SP-A but not of SP-B in BALF were reduced. Minimum surface-tension values approached 0 mN/m in controls, and ranged from 10 to 25 mN/m in the absence of supernatant protein and from 20 to 35 mN/m in recombination with leaked protein in the groups with ARDS and/or PNEU. Abnormalities in alveolar PNEU surpassed those in bronchial PNEU, and interstitial PNEU presented a distinct pattern with extensive metabolic changes. All surfactant changes were absent in CLE except for a slight inhibition of surface activity by proteins. We conclude that pronounced surfactant abnormalities, comparable to those in ARDS in the absence of lung infection, occur in different entities of severe PNEU, but not in CLE.
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In acute illness, the normally nutrient-poor alveolus is flooded with nutrient-rich oedema, oxygen and temperature gradients are established, and host stress signalling molecules selectively promote the growth of potential pathogens.
“The normally nutrient-poor environment of the alveolus is flooded with nutrient-rich oedema,55 pockets of oxygen and heterogeneous temperature gradients are established,48,49 and the signalling molecules of the host stress response selectively promote the growth of potential pathogens.”
From The microbiome and critical illness (2016) · cites this paper as [55]
Inactivation of alveolar surfactant decreases the elimination of surfactant-sensitive bacteria.
“The inactivation of alveolar surfactant decreases the elimination of surfactant-sensitive bacteria.”
From The microbiome and critical illness (2016) · cites this paper as [55]
Many daily therapies and interventions in intensive care increase intestinal permeability, bacterial translocation, and bacterial virulence.
“Many daily therapies and interventions in intensive care increase intestinal permeability (eg, nonsteroidal anti-inflammatory drugs109 and parenteral feeding55,82), bacterial translocation (eg, antibiotics,65 corticosteroids,110 and opiates111), and bacterial virulence (eg, opiates19 and catecholamines22,51).”
From The microbiome and critical illness (2016) · cites this paper as [55]
In alveolar injury, the bactericidal surfactant layer is inactivated and microbial elimination is slowed by impairment of mucociliary clearance.
“The bactericidal surfactant layer is inactivated55,57 and microbial elimination is slowed by impairment of mucociliary clearance.”
From The microbiome and critical illness (2016) · cites this paper as [55]
The microbiome and alveolar injury can propel each other in a dysregulated feedback loop that spans the host-microbiome divide.
“The microbiome and alveolar injury can propel each other in a dysregulated feedback loop that spans the host–microbiome divide”
From The microbiome and critical illness (2016) · cites this paper as [55]
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The microbiome and critical illness
Dickson, R. P. (2016) · The Lancet Respiratory Medicine · doi:10.1016/s2213-2600(15)00427-0 · Cited by 460 · see citing works
- Authors
- Günther, A., Siebert, C., Schmidt, R., Ziegler, S., Grimminger, F., Yabut, M., Temmesfeld, B., Walmrath, D., Morr, H., & Seeger, W.
- Affiliations
- Justus-Liebig-Universität Gießen (DE)
- Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 1996-01-01
- Volume
- 153
- Issue
- 1
- Pages
- 176-184
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2166443939
- Cited by
- 417
- References
- 7
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 11 · 2023: 8 · 2022: 7 · 2021: 9 · 2020: 11 · 2019: 13 · 2018: 10 · 2017: 15 · 2016: 7 · 2015: 11 · 2014: 18 · 2013: 11 · 2012: 8
- FWCI
- 20.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory and Critical Care Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Keywords
- acute respiratory distress syndrome, severe pneumonia, bronchoalveolar lavage fluid, phospholipids, phosphatidylcholine, phosphatidylglycerol, phosphatidylinositol, sphingomyelin, surfactant apoprotein, surfactant protein A, surfactant protein B, surface tension, mechanical ventilation
- MeSH terms
- Acute Disease, Adolescent, Adult, Aged, Apoproteins, Biochemical Phenomena, Biochemistry, Biophysics, Bronchoalveolar Lavage Fluid, Cell Count, Data Interpretation, Statistical, Heart Failure, Humans, Middle Aged, Phospholipids, Pneumonia, Pulmonary Edema, Pulmonary Surfactants, Respiratory Distress Syndrome, Surface Tension, Biophysical Phenomena
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