Macrophages lung disease

Fig.l. Expression of CC and CXC chemokine receptors by inflammatory and structural cells in allergic lung disease. Eos, eosinophil Mac, macrophage Mono, monocyte. 

Respiratory allergies and infections are the most common form of illness in the United States and Europe and account for more missed school and work days than any other disease [1], A substantial body of experimental work has clearly shown that airborne toxicants such as tobacco smoke, ozone, and other air pollutants can alter many aspects of the host defense network to either decrease resistance to infection, or exacerbate respiratory allergies and asthma [2], Exposure to air toxicants can suppress a number of key host defenses including mucociliary clearance in the airways, pulmonary macrophage function, and development of specific immune responses such as IgG antibody production and cell mediated immunity. In contrast, immune stimulation in the form of increased T cell activity and IgE antibody formation has also has been shown to occur under some circumstances, resulting in increased incidence or severity of allergic lung disease. 

Lasky JA, Bonner JC, Brody AR. 1991. The pathobiology of asbestos-induced lung disease A proposed role for macrophage-derived growth factors. Aim NY Acad Sci 239-244. 

Nagai S., Aung, H., Takeuchi, M., Kusume, K. and Izumi, T. (1991). IL-1 and IL-1 inhibitory activity in the culture supernatants of alveolar macrophages from patients with interstitial lung diseases. Chest 99, 674-680. 

Poulter, L.W. (1990). Changes in lung macrophages during disease. FEMS Micro. Immunol. 64, 327-332. 

Janson, R.W., King, T.E. Jr., Hance, K.R. and Arend, W.P. (1993). Enhanced production of IL-1 receptor antagonist by alveolar macrophages from patients with interstitial lung disease. Am. Rev. Respir. Dis. 148, 495-503. 

Rennard, S.L, Hunninghake, G.W., Bitterman, P.B. and Crystal, R.G. (1981). Production of fibronectin by the human alveolar macrophage mechanism for the recruitment of fibroblasts to sites of tissue injury in interstitial lung diseases. Proc. Natl. Acad. Sci. USA 78, 7147-7151. 

Standiford, T.J., Rolfe, M.W., Kunkel, S.L. et al. (1993). Macrophage inflammatory protein-1 alpha expression in interstitial lung disease. J. Immunol. 151, 2852-2863. 

So far, we have talked mostly about neoplastic diseases. What about the effects of POM on non-neoplastic diseases Here very little information is available, although there is clear evidence that inhalation of particles can effect the macrophage population and induce processes which may be important in the production of emphysema and other chronic obstructive lung diseases. Immunological consequences of POM exposure have hardly been studied and are little understood today. 

Martinez JA, King TE Jr, Brown K, Jennings CA, Borish L, Mortenson RL, Khan TZ, Bost TW, Riches DW. Increased expression of the interleukin-10 gene by alveolar macrophages in interstitial lung disease. Am J Physiol 1997 273 L676. 

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