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August 1, 1974Journal of Clinical InvestigationOpen Access

Acute Immunologic Pulmonary Alveolitis

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Authors

KJKent J. JohnsonUniversity of Michigan
Peter A. Ward
Peter A. WardUniversity of Warwick

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Implication

Animal study reveals that acute immunologic lung injury requires neutrophils and complement C3 in rats, highlighting mechanisms driving immune complex alveolitis.

Key Points

  • To characterize the development of acute immunologic lung injury and identify the specific cellular and humoral mediators driving tissue damage.
  • Induced acute lung injury in rats using intrabronchial injection of heterologous antibody combined with intravenous radiolabeled antigen.
  • Quantified pulmonary damage via vascular permeability and extractable hemoglobin, while tracking antigen, antibody, and circulating radiolabeled C3 using immunofluorescence and tissue counts.
  • Performed cellular and complement ablation experiments to test the necessity of circulating neutrophils and C3.
  • Produced an acute hemorrhagic, neutrophil-rich alveolar and interstitial exudate within 4 hours that subsequently faded.
  • Detected antigen and antibody deposits in alveolar and interstitial spaces without direct local C3 deposition, although circulating radiolabeled C3 accumulated in injured tissue.
  • Demonstrated that depleting either circulating neutrophils or complement component C3 prevents the development of acute immune-mediated lung injury.

Cite This Study

Johnson et al. (1974) studied this question.

synapsesocial.com/papers/6a6f6ef878a11c550e09239fhttps://doi.org/10.1172/jci107770
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