Santon Thaver1, Ellen J Bennett1, Lisa Foa1, Stephen M Richards1, A Bruce Lyons1, Graeme R Zosky2. 1. School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia. 2. School of Medicine, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia; Menzies Institute for Medical Research, College of Health and Medicine, University of Tasmania, Hobart, Tasmania, Australia. Electronic address: Graeme.Zosky@utas.edu.au.
Abstract
BACKGROUND: Little is known about the effect of pregnancy on the response to particulate matter. The aim of this study was to determine if pregnancy increases the susceptibility to PM from different sources using a mouse model. METHODS: Pregnant, eight-week-old C57BL/6J mice were exposed intranasally to 50 μg of diesel exhaust particles (DEP), iron oxide (Fe2O3) or silica (SiO2) in 50 μL of saline, or saline alone, on gestational day (E)7.5, E12.5 and E17.5. Groups of non-pregnant mice were exposed on day (D)0, D5 and D10. Biological samples were collected 24 h after the last exposure. Serum IL-4 and IL-6 levels were quantified by ELISA. Bronchoalveolar lavage (BAL) fluid was collected for inflammatory cells counts and assessment of IFN-ɣ, IL-4, IL-5, IL-6, IL-8 and IL-10 levels by ELISA. The spleen and thymus were also collected and the percentage of B cells and CD4+, CD8+ and CD4+CD25 + T cells were determined by flow cytometry. RESULTS: Exposure to silica caused an influx of lymphocytes, eosinophils and neutrophils into the lung. The magnitude of this response was suppressed by pregnancy. Pregnancy also enhanced the production of CD4+CD25 + T cells in response to DEP and silica exposure. CONCLUSIONS: Collectively, our data suggest that pregnancy reduces the inflammatory response to silica and alters the immune response to DEP. These responses were accompanied by pregnancy related changes including increased IL-4 production, reduced IL-8 production and an increase in the proportion of CD4+CD25 + T cells in response to PM exposure.
BACKGROUND: Little is known about the effect of pregnancy on the response to particulate matter. The aim of this study was to determine if pregnancy increases the susceptibility to PM from different sources using a mouse model. METHODS: Pregnant, eight-week-old C57BL/6J mice were exposed intranasally to 50 μg of diesel exhaust particles (DEP), iron oxide (Fe2O3) or silica (SiO2) in 50 μL of saline, or saline alone, on gestational day (E)7.5, E12.5 and E17.5. Groups of non-pregnant mice were exposed on day (D)0, D5 and D10. Biological samples were collected 24 h after the last exposure. Serum IL-4 and IL-6 levels were quantified by ELISA. Bronchoalveolar lavage (BAL) fluid was collected for inflammatory cells counts and assessment of IFN-ɣ, IL-4, IL-5, IL-6, IL-8 and IL-10 levels by ELISA. The spleen and thymus were also collected and the percentage of B cells and CD4+, CD8+ and CD4+CD25 + T cells were determined by flow cytometry. RESULTS: Exposure to silica caused an influx of lymphocytes, eosinophils and neutrophils into the lung. The magnitude of this response was suppressed by pregnancy. Pregnancy also enhanced the production of CD4+CD25 + T cells in response to DEP and silica exposure. CONCLUSIONS: Collectively, our data suggest that pregnancy reduces the inflammatory response to silica and alters the immune response to DEP. These responses were accompanied by pregnancy related changes including increased IL-4 production, reduced IL-8 production and an increase in the proportion of CD4+CD25 + T cells in response to PM exposure.