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T cell independence of bleomycin‐induced pulmonary fibrosis
Author(s) -
Helene M.,
LakeBullock V.,
Zhu J.,
Hao H.,
Cohen D. A.,
Kaplan A. M.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.65.2.187
Subject(s) - bleomycin , pulmonary fibrosis , hydroxyproline , fibrosis , biology , pathology , severe combined immunodeficiency , inflammation , lung , immunology , ratón , medicine , in vivo , endocrinology , chemotherapy , genetics , microbiology and biotechnology
The role of T cells and cytokines in bleomycin (BLM)‐induced fibrosis was evaluated in susceptible and resistant strains of normal and SCID mice. Histology and hydroxyproline analysis showed that BLM induced pulmonary fibrosis in C57BL/6 and (C57BL/6 × BALB/c)F 1 mice, whereas BALB/c mice were resistant to the disease. To test whether lymphocytes were required for the induction of BLM‐induced pulmonary fibrosis, SCID mice were injected intratracheally with BLM and evaluated for the development of pulmonary inflammation and fibrosis. Similar morphological changes and increases in hydroxyproline were observed in both C57BL/6 SCID and (C57BL/6 × CB.17)F 1 SCID animals compared to those seen in wild‐type C57BL/6 and (C57BL/6 × BALB/c)F 1 mice. In contrast, CB.17 SCID mice, which are genetically similar to BALB/c mice, were resistant to disease induction. Analysis of the cellular infiltrate in BLM‐treated C57Bl/6 SCID mice confirmed a lack of T cells in the lungs of SCID mice and demonstrated a pronounced accumulation of eosinophils in areas of developing pulmonary fibrosis. NK cells were significantly elevated in untreated SCID mice and did not increase further after BLM treatment. Analysis of selected cytokines 1 day after initiation of BLM‐induced pulmonary fibrosis indicated that the levels of TNF‐α and IFN‐γ appeared to segregate with fibrosis in both the SCID and wild‐type mice. The data demonstrate that T cells are not required for the induction of fibrosis by BLM and suggest that responses by non‐lymphoid cells may be sufficient for the induction of fibrosis. J. Leukoc. Biol. 65: 187–195; 1999.

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