Rheumatology Advance Access originally published online on June 18, 2007
Rheumatology 2007 46(9):1405-1410; doi:10.1093/rheumatology/kem117
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Characterization of haemorrhagic pulmonary capillaritis: another manifestation of Pristane-induced lupus
Division of Rheumatology, Department of Medicine, 1Division of Laboratory Medicine and Pathology and 2Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Correspondence to: Chella S. David, PhD, Professor of Immunology, Department of Immunology, Mayo Clinic College of Medicine, 200, 1st SW Rochester, MN 55905, USA. E-mail: davic4{at}mayo.edu
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Abstract |
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Objectives. Pristane-induced lupus is a well-established model of murine lupus. Mice injected with Pristane develop lupus-specific autoantibodies and glomerulonephritis. A chance observation led us to identify and characterize haemorrhagic pulmonary capillaritis in Pristane-injected mice.
Methods. Eight-week-old C57Bl/10 (B10, H-2b) mice received a single intraperitoneal injection of 0.5 ml of Pristane. Control mice received phosphate-buffered saline (PBS) injection. Mice were bled at 2 weeks after Pristane injection and monthly thereafter for serology and for antinuclear antibody (ANA). To characterize pulmonary disease, bronchoalveolar lavage (BAL) was carried out for total and differential cell count. Cytokines levels were checked for IL-2, IL-4, TNF-
, IFN-
, IL-6 and IL-10. Lungs were examined by histopathology and electron microscopy.
Results. All mice injected with Pristane developed a pulmonary capillaritis with perivascular infiltration with macrophages, neutrophils, lymphocytes and eosinophils. In addition, alveoli showed macrophage and neutrophil infiltration. The degree of perivascular and alveolar inflammation was moderate to severe. BAL was inflammatory with cell composition of macrophages, neutrophils, lymphocyte and eosinophils. There was evidence of endothelial injury on electron microscopy but no evidence of immune complex deposition. IL-6 and IL-10 were increased in BAL but levels of TNF-, IFN-, IL-2 and IL-4 were not. Anti-neutrophil cytoplasm antibody (ANCA) was negative. Kidneys demonstrated an increase in mesangial matrix and cellularity compatible with WHO Class II lupus lesion. There were immune complexes and complement deposition in the kidney. There were oil granulomas in peritoneum, spleen and liver but no evidence of vasculitis in these organs was seen.
Conclusion. The relative ease and high penetrability of lesion makes it an attractive model to study pulmonary vasculitis.
KEY WORDS: Pristane induced lupus, pulmonary vasculitis
Submitted 25 January 2007;
revised version accepted 27 March 2007.
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