Bronchoalveolar macrophages in sarcoidosis and cryptogenic fibrosing alveolitis

Abstract

Summary Previous reports suggest that blood monocytes and tissue epithelioid cells in patients with sarcoidosis are‘activated’, but few studies have been undertaken on human alveolar macrophages. In the present study, bronchoulveolar lavage samples have been obtained from eighteen patients with sarcoidosis and these have been compared with twenty controls and twenty‐nine patients with non‐granulomatous chronic inflammatory interstitial lung disease (cryptogenic fibrosing alveolitis). Assessment of the functional state of the macrophages was made by measurements of C3b receptor sites on the cell membrane, intra and extracellular lysosomal enzyme (β‐D‐glucosaminidase) and the degree of spreading of macrophages on glass. C3b receptor sites and intracellular levels of lysosomal enzyme were significantly reduced in sarcoidosis compared to controls; levels of extracellular enzyme in the lavage supernatant fluid and macrophage spreading were similar to controls. These features suggest that alveolar macrophages from patients with sarcoidosis are not “activated”. By contrast, in cryptogenic fibrosing alveolitis. macrophages show a greater extracellular intracellular ratio of lysosomal enzyme and more spreading, suggestive of ‘activation’.

Allergic lung responses are increased in prostaglandin H synthase–deficient mice

“…To explore whether the allergen-induced inflammation in the PGHS-1 -/-and PGHS-2 -/-mice was accompanied by increased lysosomal enzyme release, we measured BAL fluid NAG, an established marker of alveolar macrophage activation (28). Compared with allergic wild-type mice, allergic PGHS-1 -/-mice exhibited a 3-fold increase in BAL fluid NAG (P < 0.001 vs. allergic wild-type mice), and allergic PGHS-2 -/-mice had a 2-fold increase in BAL fluid NAG (P < 0.005 vs. allergic wild-type mice; P < 0.01 vs. allergic PGHS-1 -/-mice) (Figure 3b).…”