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Pristane‐induced alveolar hemorrhage in C57BL/6 mice is not mediated by immune complex, T or B‐cells, or Fas
Author(s) -
Barker Tolga,
Lee Pui Y.,
Weinstein Jason S.,
Nacionales Dina C.,
KellyScumpia Kindra M.,
Sobel Eric S.,
Reeves Westley H.,
Satoh Minoru
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.668.24
Subject(s) - pristane , systemic lupus erythematosus , immunology , immune system , apoptosis , chemistry , spleen , antibody , medicine , biochemistry , hydrocarbon , organic chemistry , disease
Intraperitoneal (ip) injection of pristane in normal mice induces antinuclear antibodies and immune‐complex (IC) glomerulonephritis similar to human systemic lupus erythematosus (SLE). In addition, C57BL/6 (B6) mice frequently develop alveolar hemorrhage (AH), leading to 10–50% early mortality. AH is an uncommon but often fatal complication of human SLE and is thought to be mediated by IC. The role of IC, apoptosis and T‐ and B‐cells in pristane‐induced AH was investigated. B6, B6 RAG1−/−, B6 FcR γ1 −/−, and B6/ lpr , received ip pristane and the lungs were examined for pathology, IC deposition, apoptosis and cytokines and chemokines. In some experiments, bone marrow, spleen, or peritoneal cells from pristane‐treated B6 mice were transferred to RAG1−/− mice to examine their ability to induce AH. Two‐weeks after pristane ip, nearly all of B6, B6 RAG1−/− or B6 FcRγ1 −/− mice developed AH, indicating IC, autoantibody‐binding to lung tissue, or T‐ or B‐cells is not necessary for AH. B6/ lpr are resistant to pristane‐induced lupus yet developed AH, indicating that Fas‐mediated apoptosis is not essential and that AH and other pathology induced by pristane are regulated differently. Short term transfer of pristane treated B6 cells into RAG1−/− mice did not induce AH while some long term transfers did induce AH. We conclude that the induction of AH by pristane does not require IC or antibodies, B‐ or T cells, or Fas. Supported by NIH.