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Updated: Jun 22, 2026
A Method for Generating Pulmonary Neutrophilia Using Aerosolized Lipopolysaccharide
Published on: December 15, 2014
Inhaled endotoxin induces a systemic neutrophil response without affecting cardiovascular measures in a randomized
Stephen A Schworer1,2,3, Alan L Hinderliter4, Melissa C Caughey5
1Division of Allergy and Immunology, Department of Pediatrics, UNC School of Medicine, University of NC at Chapel Hill, NC, USA.
Objective:
The gram-negative bacterial cell wall component endotoxin (lipopolysaccharide, LPS) is a key component of particulate matter (PM). PM exposure is associated with cardiovascular morbidity and mortality. However, the contribution of individual components of PM to acute and chronic cardiovascular measures is not clear. This study examines whether systemic inflammation induced by LPS inhalation causes acute changes in cardiovascular physiology measures.
Materials And Methods:
In this double blinded, placebo-controlled crossover study, fifteen adult volunteers underwent inhalation exposure to 20,000 EU Clinical Center Reference Endotoxin (CCRE). Peripheral blood and induced sputum neutrophils were obtained at baseline and six hours post-exposure. Blood pressure, measures of left ventricular function (ejection fraction (LVEF) and global longitudinal strain (LVGLS)), and indices of endothelial function (flow mediated dilation (FMD) and velocity time integral during hyperemia (VTIhyp)) were measured before and after treatment. Wilcoxon sign-rank tests and linear mixed models were used for statistical analysis.
Results:
In comparison with normal saline, LPS inhalation resulted in significant increases in peripheral blood and sputum neutrophils but was not associated with significant alterations in blood pressure, LVGLS, LVEF, FMD, or VTIhyp.
Discussion And Conclusions:
In healthy adults, systemic inflammation after LPS inhalation was not associated with acute changes in cardiovascular physiology. Larger studies are needed to investigate the effects of other PM components on inflammation induced cardiovascular dysfunction.
Insights
Inhalation of lipopolysaccharide (LPS) caused systemic inflammation in healthy adults but did not acutely affect cardiovascular measures. Further research is needed on particulate matter components and cardiovascular health.
Area of Science:
- Environmental Health
- Cardiovascular Physiology
- Immunology
Background:
- Particulate matter (PM) exposure is linked to cardiovascular disease.
- Lipopolysaccharide (LPS), a component of PM, may contribute to cardiovascular effects.
- The acute impact of LPS-induced inflammation on cardiovascular function is not well understood.
Purpose of the Study:
- To investigate if LPS inhalation causes acute changes in cardiovascular physiology measures in healthy adults.
- To assess the systemic inflammatory response to LPS exposure.
Main Methods:
- A double-blinded, placebo-controlled crossover study involving fifteen adult volunteers.
- Inhalation exposure to LPS (20,000 EU CCRE) or placebo.
- Measurements of blood pressure, left ventricular function (LVEF, LVGLS), and endothelial function (FMD, VTIhyp) pre- and post-exposure.
- Analysis of peripheral blood and sputum neutrophils.
Main Results:
- LPS inhalation significantly increased peripheral blood and sputum neutrophils, indicating systemic inflammation.
- No significant alterations were observed in blood pressure, LVGLS, LVEF, FMD, or VTIhyp post-LPS exposure.
- The inflammatory response did not translate to acute cardiovascular physiological changes.
Conclusions:
- Systemic inflammation induced by LPS inhalation does not acutely alter cardiovascular physiology in healthy adults.
- Other components of particulate matter may play a role in inflammation-induced cardiovascular dysfunction.
- Larger studies are warranted to explore the long-term and component-specific effects of PM on cardiovascular health.
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