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Related Experiment Video

Updated: May 29, 2026

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

Novel proresolving aspirin-triggered DHA pathway.

Charles N Serhan¹, Gabrielle Fredman, Rong Yang

¹Center for Experimental Therapeutics and Reperfusion Injury, Harvard Institutes of Medicine, Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02115, USA. cnserhan@zeus.bwh.harvard.edu

Chemistry & Biology

|August 27, 2011

Summary

This summary is machine-generated.

Aspirin triggers the creation of a novel anti-inflammatory molecule, aspirin-triggered Neuroprotectin D1 (AT-NPD1). This molecule effectively reduces neutrophil recruitment and enhances the clearance of inflammatory cells, promoting inflammation resolution.

Related Experiment Videos

Last Updated: May 29, 2026

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

A Model of Self-limited Acute Lung Injury by Unilateral Intra-bronchial Acid Instillation

Published on: August 30, 2019

Area of Science:

Biochemistry
Immunology
Pharmacology

Background:

Excessive inflammation is implicated in numerous pathological conditions.
Understanding endogenous mechanisms for resolving acute inflammation is crucial.

Purpose of the Study:

To identify and characterize novel endogenous molecules involved in inflammation resolution.
To investigate the anti-inflammatory and proresolving properties of aspirin-triggered docapentaenoic acid (DHA) metabolites.

Main Methods:

Biosynthesis and isolation of aspirin-triggered Neuroprotectin D1 (AT-NPD1) from inflammatory exudates and human leukocytes.
Determination of the complete stereochemistry of AT-NPD1 using organic synthesis and biological material comparison.
Evaluation of AT-NPD1's effect on neutrophil recruitment in murine peritonitis models.
Assessment of AT-NPD1's impact on transendothelial neutrophil migration and efferocytosis in human cell cultures.

Main Results:

Aspirin triggers the biosynthesis of AT-NPD1, a potent anti-inflammatory molecule with specific stereochemistry.
AT-NPD1 significantly reduced neutrophil recruitment in vivo and transendothelial migration in vitro.
AT-NPD1 enhanced the efferocytosis of apoptotic neutrophils by macrophages.

Conclusions:

AT-NPD1 is a potent endogenous proresolving lipid mediator.
The stereochemistry of AT-NPD1 is essential for its bioactivity.
AT-NPD1 represents a promising therapeutic target for managing inflammatory diseases.