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Related Experiment Videos

Neurogenic amplification of immune complex inflammation

C R Bozic1, B Lu, U E Höpken

  • 1Perlmutter Laboratory, Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.

Science (New York, N.Y.)
|September 20, 1996
PubMed
Summary

Intrapulmonary immune complexes trigger lung inflammation. Blocking the substance P receptor (NK-1R) or C5a receptor protected mice from this injury, suggesting substance P

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Area of Science:

  • Immunology
  • Pulmonary Medicine
  • Inflammation Research

Background:

  • Intrapulmonary immune complex formation initiates a significant inflammatory cascade.
  • This response involves increased microvascular permeability and neutrophil infiltration in the lungs.

Purpose of the Study:

  • To investigate the role of substance P and its receptor (NK-1R) in immune complex-induced lung inflammation.
  • To determine the involvement of the C5a anaphylatoxin receptor in this inflammatory process.

Main Methods:

  • Utilizing gene-targeted disruption in mice to study the effects of receptor knockout.
  • Measuring substance P levels in lung lavage fluids.
  • Assessing inflammatory responses, including microvascular permeability and neutrophil influx.

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Main Results:

  • Gene-targeted disruption of the substance P receptor (NK-1R) conferred protection against lung injury.
  • Disruption of the C5a anaphylatoxin receptor also protected the lung from immune complex-induced damage.
  • Immunoreactive substance P was detected in lung fluids prior to neutrophil influx.

Conclusions:

  • The substance P receptor (NK-1R) and C5a receptor play critical roles in immune complex-mediated lung inflammation.
  • Substance P may be involved in the early stages of the lung's inflammatory response to immune complexes.