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Updated: May 2, 2026

Intra-tracheal Administration of Haemophilus influenzae in Mouse Models to Study Airway Inflammation
Published on: March 2, 2016
High-density lipoprotein loses its anti-inflammatory properties during acute influenza a infection
B J Van Lenten1, A C Wagner, D P Nayak
1Department of Medicine, UCLA School of Medicine, Los Angeles, California, USA. bvanlent@mednet.ucla.edu
Background:
Viruses have been identified as one of a variety of potential agents that are implicated in atherogenesis.
Methods And Results:
C57BL/6J mice were killed before or 2, 3, 5, 7, or 9 days after intranasal infection with 10(5) plaque-forming units (pfu) of Influenza A strain WSN/33. Peak infectivity in lungs was reached by 72 hours, and it returned to baseline by 9 days. No viremia was observed at any time. The activities of paraoxonase and platelet-activating factor acetylhydrolase in HDL decreased after infection and reached their lowest levels 7 days after inoculation. The ability of HDL from infected mice to inhibit LDL oxidation and LDL-induced monocyte chemotactic activity in human artery wall cell cocultures decreased with time after inoculation. Moreover, as the infection progressed, LDL more readily induced monocyte chemotaxis. Peak interleukin-6 and serum amyloid A plasma levels were observed at 2 and 7 days after inoculation. HDL apoA-I levels did not change. ApoJ and ceruloplasmin levels in HDL peaked 3 days after infection. Ceruloplasmin remained elevated throughout the time course, whereas apoJ levels decreased toward baseline after the third day.
Conclusions:
We conclude that alterations in the relative levels of paraoxonase, platelet-activating factor acetylhydrolase, ceruloplasmin, and apoJ in HDL occur during acute influenza infection, causing HDL to lose its anti-inflammatory properties.
Insights
Influenza infection alters high-density lipoprotein (HDL) composition, reducing its anti-inflammatory capacity. This study investigated changes in HDL during acute influenza in mice.
Area of Science:
- Cardiovascular Science
- Virology
- Immunology
Background:
- Viruses are implicated in the development of atherosclerosis.
- Influenza A virus infection serves as a model to study viral impact on cardiovascular health.
Purpose of the Study:
- To investigate the effects of acute influenza infection on high-density lipoprotein (HDL) functionality.
- To determine how influenza impacts HDL's anti-atherogenic properties.
Main Methods:
- C57BL/6J mice were infected intranasally with Influenza A strain WSN/33.
- Analysis of HDL components (paraoxonase, platelet-activating factor acetylhydrolase, apoA-I, apoJ, ceruloplasmin) and functionality (inhibition of LDL oxidation, monocyte chemotaxis) at various time points post-infection.
- Measurement of plasma inflammatory markers (interleukin-6, serum amyloid A).
Main Results:
- Influenza infection led to decreased activities of paraoxonase and platelet-activating factor acetylhydrolase in HDL.
- HDL's ability to inhibit LDL oxidation and monocyte chemotaxis was reduced post-infection.
- Plasma levels of interleukin-6 and serum amyloid A increased, indicating an inflammatory response.
Conclusions:
- Acute influenza infection alters HDL composition, specifically affecting paraoxonase, platelet-activating factor acetylhydrolase, ceruloplasmin, and apoJ levels.
- These HDL alterations result in a loss of its anti-inflammatory properties.
- Influenza-induced changes in HDL may contribute to atherogenesis.
Related Concept Videos
Inflammation
Influenza
Inhibitors of Viral Protein Synthesis
Acute Inflammation I: Inflammatory Response
Acute Inflammation I: Cellular Phase
Acute Inflammation II: Local and Systemic Effects

