Functional studies on macrophage populations in the airways and the lung wall of SPF mice in the steady-state and during respiratory virus infection

• Published in: Immunology 1988-11, Vol.65 (3), p.417-425
• Main Authors: BILYK, N, MACKENZIE, J. S, PAPADIMITRIOU, J. M, HOLT, P. G
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Bronchoalveolar Lavage Fluid - immunology; Cell Count; Cells, Cultured; Female; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Germ-Free Life; Immunobiology; influenza virus; Macrophage Activation; Macrophages - immunology; Mice; Mice, Inbred CBA; Myeloid cells: ontogeny, maturation, markers, receptors; Orthomyxoviridae Infections - immunology; Specific Pathogen-Free Organisms; T-Lymphocytes - immunology
• ISSN: 0019-2805; 1365-2567

Collagenase digestion of slices of lavaged and perfused murine lung from SPF animals yielded, on average, 104 x 10(6) mononuclear cells per gram tissue, including approximately 14% F4/80+ macrophages and 35% lymphocytes. The lung tissue-associated (digest) macrophage (LDM) population was 10-fold higher in number than the alveolar macrophage (AM) population recoverable by lavage. Comparative functional analysis of these populations was performed, employing assays for immune receptors (Fc and C3), complement-induced spreading, endogenous peroxidase, IL-1 secretion and tumour cytolysis; resident and activated peritoneal macrophages and blood monocytes were examined in parallel. The resident LDM population exhibited an activation status intermediate between blood monocytes and the relatively more activated AM from the airways. Murine lung macrophages were also examined during an acute influenza infection and LDM and AM recoveries increased significantly. The AM population exhibited activation during an acute infection. In contrast, LDM remained quiescent, despite the influx of a large number of T lymphocytes into the lung wall. These results suggest that LDM may be intrinsically resistant to the signals generated during T-cell-mediated eradication of influenza, or else local tissue factors modulate T-cell-derived activation signals.