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Updated: Jun 23, 2026

Direct Observation of Phagocytosis and NET-formation by Neutrophils in Infected Lungs using 2-photon Microscopy
08:50

Direct Observation of Phagocytosis and NET-formation by Neutrophils in Infected Lungs using 2-photon Microscopy

Published on: June 2, 2011

Human neutrophil peptides and phagocytic deficiency in bronchiectatic lungs

Stefanos Voglis1, Kieran Quinn, Elizabeth Tullis

  • 1The Keenan Research Centre, Li Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, Ontario, Canada.

American Journal of Respiratory and Critical Care Medicine
|May 2, 2009
PubMed
Abstract

Insights

Human neutrophil peptides (HNP) in cystic fibrosis (CF) lungs impair neutrophil function, explaining persistent bacterial infections. This interaction suggests HNP as a therapeutic target for inflammatory lung diseases.

Area of Science:

  • Immunology
  • Pulmonology
  • Microbiology

Background:

  • Cystic fibrosis (CF) patients exhibit persistent lung bacterial infections despite abundant neutrophils and human neutrophil peptides (HNP).
  • The mechanisms behind this clinical paradox, where expected antimicrobial agents fail, remain unclear.

Purpose of the Study:

  • To investigate the mechanisms underlying the paradox of persistent bacterial infections in CF lungs.
  • To examine the interaction between neutrophils and HNP and its effect on bacterial clearance.

Main Methods:

  • Polymorphonuclear neutrophils (PMN) were isolated from CF and non-CF bronchiectasis patients' sputum and blood.
  • Phagocytic assays were performed on isolated PMN and on healthy PMN stimulated with HNP from CF patients.
  • Animal models (Pallid mice) were used to study HNP effects on PMN lung infiltration and phagocytosis.

Main Results:

  • PMN from bronchiectatic patients' sputum showed defective phagocytosis, correlating with high lung HNP concentrations.
  • Incubation of healthy PMN with HNP reduced phagocytic capacity by affecting Fc gamma RIII, actin remodeling, intracellular Ca(2+), and degranulation.
  • HNP-induced phagocytic deficiency was mitigated by blocking intracellular Ca(2+) or using alpha1-proteinase inhibitor; HNP instillation in mice led to increased PMN infiltration and phagocytic deficiency.

Conclusions:

  • The interaction between HNP and PMN diminishes their individual antimicrobial capabilities, explaining the paradox in CF and other inflammatory lung diseases.
  • Human neutrophil peptides (HNP) represent a potential novel therapeutic target for managing persistent lung infections in inflammatory lung diseases.

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