Faculty Collaboration Database

The role of complement in experimental silicosis. Environ Res 1986 Aug;40(2):301-12

Date

08/01/1986

Pubmed ID

3015583

DOI

10.1016/s0013-9351(86)80105-0

Scopus ID

2-s2.0-0022516884 (requires institutional sign-in at Scopus site)   14 Citations

Abstract

The role of the complement system in the pathogenesis of crystal-induced pulmonary inflammation and fibrosis was evaluated using a mouse model of silicosis and congenitally complement-deficient mice. Mice lacking the fifth component of complement (B10.D2/o) were compared to C5-sufficient animals (B10.D2/n) for pulmonary changes following intratracheal instillation of silica crystals. Complement-deficient mice demonstrated a significant reduction compared to complement-sufficient mice in both cell number and protein content of lung lavage fluid throughout the 12 weeks following silica exposure. Lung hydroxyproline content (indicative of collagen deposition) was equivalent for both strains and significantly higher than controls at all time points following silica instillation. Moreover, studies in vitro have shown that silica crystals are capable of activating complement via the alternative pathway. These studies indicate that the complement system may be responsible for some of the pulmonary inflammation, but not fibrosis elicited by silica exposure.

Author List

Callis AH, Sohnle PG, Mandel GS, Mandel NS

MESH terms used to index this publication - Major topics in bold

Animals
Complement Activation
Complement C3
Complement C5
Female
Hydroxyproline
Lung
Male
Mice
Silicon Dioxide
Silicosis