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Rat alveolar and interstitial macrophages in the fibrosing stage following quartz exposure

Department of Medicine, Division of Respiratory Medicine, Karolinska Hospital, S-171 76, Stockholm Sweden

G Elmberger

Department of Pathology and Cytology, Karolinska Hospital, S-171 76, Stockholm Sweden

A Johansson

Division of Inhalation Toxicology, Institute of Environmental Medicine, Karolinska Institute, S-171 77, Stockholm Sweden; The WennerGren Institute, University of Stockholm, S-106 91, Stockholm Sweden

J Lundahl

Department of Clinical Immunology, Karolinska Hospital, S-171 76, Stockholm Sweden

M Lundborg

Division of Inhalation Toxicology, Institute of Environmental Medicine, Karolinska Institute, S-171 77, Stockholm Sweden

C M Sköld

G Tornling

Department of Medicine, Division of Respiratory Medicine, Karolinska Hospital, S-171 76, Stockholm Sweden

P Camner

Division of Inhalation Toxicology, Institute of Environmental Medicine, Karolinska Institute, S-171 77, Stockholm Sweden

A Eklund

Department of Medicine, Division of Respiratory Medicine, Karolinska Hospital, S-171 76, Stockholm Sweden

Exposure to quartz induces pulmonary inflammation and development of fibrosis. In order to study the fibrosing process, we investigated morphology function and phenotype of alveolar (AMs) and interstitial (IMs) macrophages at an early stage of fibrosis in rats.

Rats were exposed by intratracheal instillations of 10 mg quartz (n = 8) or saline (n = 8) and studied 3 months later. AMs were obtained by bronchoalveolar lavage and IMs by mechanical fragmentation, followed by enzymatic digestion of lung tissue.

Histology revealed subacute silicosis, with early focal fibrosis and alveolar lipoproteinosis. AM quartz exposure increased phagocytic activity and expression of major histocompatibility complex (MHC) Ia antigens, the latter being associated with cellular antigen presenting capacity. IM had an even more pronounced expression of MHC than AM after quartz exposure. Both macrophage fractions had a higher expression of OX-42 (complement receptor 3, CR3) than controls, but the increase in the IM fraction might be explained by the remaining AM in the IM fraction. Exposed AM adhered less to extracellular matrix components (vitronectin and fibronectin) than controls. In contrast, the adhesion of IM to vitronectin increased after exposure.

Besides increased adhesion, the effects on IM were scarce. Our results therefore do not support the hypothesis that IM has a key role in the process of inflammation, including fibrosis.

Key Words: fibrosis • inflammation • interstitium • macrophages • quartz

Human & Experimental Toxicology, Vol. 19, No. 7, 402-411 (2000)
DOI: 10.1191/096032700678816124


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