ABSTRACT
The health effects of climate change are becoming increasingly important; there are direct effects from heatwaves and floods, and indirect effects from the altered distribution of infectious diseases and changes in crop yield. Ironically, the healthcare system itself carries an environmental burden, contributing to environmental health impacts. Life cycle assessment is a widely accepted and well-established method that quantitatively evaluates environmental impact. Given that monetary evaluations have the potential to motivate private companies and societies to reduce greenhouse gas emissions using market mechanisms, instead of assessing the carbon footprint alone, we previously developed a life cycle impact assessment method based on an endpoint that integrates comprehensive environmental burdens into a single index—the monetary cost. Previous investigations estimated that therapy for chronic kidney disease had a significant carbon footprint in the healthcare sector. We have been aiming to investigate on the environmental impact of chronic kidney disease based on field surveys from the renal department in a hospital and several health clinics in Japan. To live sustainably, it is necessary to establish cultures, practices, and research that aims to conserve resources to provide environmentally friendly healthcare in Japan.
ABSTRACT
BACKGROUND/AIMS: Recent research has highlighted the importance of interactions between commensal fungi and intestinal inflammation. However, there are few studies investigating whether commensal fungi contribute to inflammation in patients with Crohn's disease (CD). The aim of this study is to investigate reveal interactions between commensal fungi and host immune cells in CD. METHODS: CD14-positive monocytes were isolated from peripheral blood mononuclear cells from healthy human volunteers and then differentiated in the presence of macrophage colony-stimulating factor (M-CSF) (referred to as M-macrophages, M-Mϕs) or M-CSF and interferon-γ (IFN-γ) (referred to as M-gamma macrophages, Mγ-Mϕs). Cytokine production by these in vitro differentiated macrophages in response to β-(1,3)-glucan was analyzed by flow cytometry. Expression of Dectin-1 was examined using flow cytometry, western blotting, and quantitative reverse transcription-polymerase chain reaction. Cytokine production by in vitro differentiated macrophages in response to β-(1,3)-glucan was measured in the presence of an anti-Dectin-1 receptor antagonist, anti-Syr, or an anti-Fas-1 antibody. Cytokine production by lamina propria mononuclear cells (LPMCs) derived from CD patients in response to β-(1,3)-glucan was also analyzed. RESULTS: Mγ-Mϕs produced a large amount of tumor necrosis factor-α (TNF-α) and interleukin-6 in response to β-(1,3)-glucan. Dectin-1 expression was significantly higher in Mγ-Mϕs than in M-Mϕs. The increase in TNF-α production by Mγ-Mϕs stimulated with glucan was reversed by blocking Dectin-1, Syr or Fas-1. LPMCs derived from CD patients stimulated with β-(1,3)-glucan produced significantly higher amount of TNF-α than LPMCs derived from UC patients. CONCLUSIONS: These results suggest that commensal fungal microbiota may contribute to the pathogenesis of CD by inducing macrophages-derived pro-inflammatory cytokines.