机构:
Mayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USAMayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USA
Villegas, Leah R.
[1
]
Kottom, Theodore J.
论文数: 0引用数: 0
h-index: 0
机构:
Mayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USAMayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USA
Kottom, Theodore J.
[1
]
Limper, Andrew H.
论文数: 0引用数: 0
h-index: 0
机构:
Mayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USA
Mayo Clin, Dept Biochem & Mol Biol, Rochester, MN 55905 USAMayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USA
Limper, Andrew H.
[1
,2
]
机构:
[1] Mayo Clin, Div Pulm & Crit Care, Dept Internal Med, Thorac Dis Res Unit, Rochester, MN 55905 USA
[2] Mayo Clin, Dept Biochem & Mol Biol, Rochester, MN 55905 USA
Pneumocystis pneumonia remains an important complication of immune suppression. The cell wall of Pneumocystis has been demonstrated to potently stimulate host inflammatory responses, with most studies focusing on beta-glucan components of the Pneumocystis cell wall. In the current study, we have elaborated the potential role of chitins and chitinases in Pneumocystis pneumonia. We demonstrated differential host mammalian chitinase expression during Pneumocystis pneumonia. We further characterized a chitin synthase gene in Pneumocystis carinii termed Pcchs5, a gene with considerable homolog to the fungal chitin biosynthesis protein Chs5. We also observed the impact of chitinase digestion on Pneumocystis-induced host inflammatory responses by measuring TNF alpha release and mammalian chitinase expression by cultured lung epithelial and macrophage cells stimulated with Pneumocystis cell wall isolates in the presence and absence of exogenous chitinase digestion. These findings provide evidence supporting a chitin biosynthetic pathway in Pneumocystis organisms and that chitinases modulate inflammatory responses in lung cells. We further demonstrate lung expression of chitinase molecules during Pneumocystis pneumonia.