September 1, 1993The Journal of Immunology
Macrophage inflammatory protein-1 alpha expression in interstitial lung disease.
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Discussion
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Implication
Observational study reveals elevated MIP-1 alpha in patients with sarcoidosis and IPF, indicating its role in recruiting and activating mononuclear phagocytes in chronic lung inflammation.
Key Points
- To investigate whether macrophage inflammatory protein-1 alpha (MIP-1 alpha) is upregulated in interstitial lung diseases and mediates the recruitment and activation of mononuclear phagocytes in sarcoidosis and idiopathic pulmonary fibrosis (IPF).
- Quantified MIP-1 alpha concentrations and monocyte chemotactic activity in bronchoalveolar lavage fluid (BALF) from patients with sarcoidosis (n=23), IPF (n=9), and healthy controls (n=7).
- Conducted immunohistochemical analysis of BAL cell pellets, transbronchial biopsies, and open lung biopsies to identify cellular sources of MIP-1 alpha.
- Assessed in vitro MIP-1 alpha production by isolated pulmonary fibroblasts exposed to interleukin-1 beta (IL-1 beta).
- MIP-1 alpha was detected in BALF from 22/23 patients with sarcoidosis (mean 443 ± 76 pg/ml) and 9/9 patients with IPF (mean 427 ± 81 pg/ml), compared to only 1/7 healthy subjects (mean 64 ± 64 pg/ml).
- BALF monocyte chemotactic activity increased 2.5-fold in sarcoidosis and 1.8-fold in IPF relative to healthy controls, and anti-MIP-1 alpha antibodies suppressed this monocyte chemotactic activity by approximately 22%.
- Immunohistochemistry identified alveolar/interstitial macrophages and interstitial fibroblasts as primary cellular sources of MIP-1 alpha in diseased lungs, and IPF fibroblasts produced greater MIP-1 alpha after IL-1 beta stimulation than non-fibrotic controls.
Cite This Study
Standiford et al. (1993) studied this question.