Reduced expression of cyclooxygenase (COX) in idiopathic pulmonary fibrosis and sarcoidosis
Aims: To test the hypothesis that cyclooxygenase (COX)‐1 or COX‐2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglan...
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| Vydáno v: | Histopathology Ročník 43; číslo 4; s. 381 - 386 |
|---|---|
| Hlavní autoři: | , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Oxford, UK
Blackwell Science Ltd
01.10.2003
Blackwell |
| Témata: | |
| ISSN: | 0309-0167, 1365-2559 |
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| Abstract | Aims: To test the hypothesis that cyclooxygenase (COX)‐1 or COX‐2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglandin E2 (PGE2) regulates collagen deposition and fibroblast proliferation and a defect in COX regulation may contribute to the fibrosis that occurs in IPF.
Methods: Immunohistochemistry was utilized to determine COX immunoreactivity in lung sections from 25 IPF, six sarcoidosis and 14 control subjects.
Results: COX‐1 and COX‐2 expression in bronchiolar epithelial cells was significantly lower in IPF and sarcoidosis than in controls. No significant difference was found in COX‐2 expression between macrophages in IPF and control sections, but COX‐2 was reduced in macrophages in sarcoidosis compared with controls.
Conclusions: These studies confirm COX‐2 loss in bronchial epithelial cells but not macrophages in IPF, and show for the first time reduced constitutive COX‐1 expression in epithelial cells and macrophages. Similar abnormalities were observed in sarcoidosis. |
|---|---|
| AbstractList | Aims: To test the hypothesis that cyclooxygenase (COX)‐1 or COX‐2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglandin E2 (PGE2) regulates collagen deposition and fibroblast proliferation and a defect in COX regulation may contribute to the fibrosis that occurs in IPF.
Methods: Immunohistochemistry was utilized to determine COX immunoreactivity in lung sections from 25 IPF, six sarcoidosis and 14 control subjects.
Results: COX‐1 and COX‐2 expression in bronchiolar epithelial cells was significantly lower in IPF and sarcoidosis than in controls. No significant difference was found in COX‐2 expression between macrophages in IPF and control sections, but COX‐2 was reduced in macrophages in sarcoidosis compared with controls.
Conclusions: These studies confirm COX‐2 loss in bronchial epithelial cells but not macrophages in IPF, and show for the first time reduced constitutive COX‐1 expression in epithelial cells and macrophages. Similar abnormalities were observed in sarcoidosis. To test the hypothesis that cyclooxygenase (COX)-1 or COX-2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglandin E2 (PGE2) regulates collagen deposition and fibroblast proliferation and a defect in COX regulation may contribute to the fibrosis that occurs in IPF.AIMSTo test the hypothesis that cyclooxygenase (COX)-1 or COX-2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglandin E2 (PGE2) regulates collagen deposition and fibroblast proliferation and a defect in COX regulation may contribute to the fibrosis that occurs in IPF.Immunohistochemistry was utilized to determine COX immunoreactivity in lung sections from 25 IPF, six sarcoidosis and 14 control subjects.METHODSImmunohistochemistry was utilized to determine COX immunoreactivity in lung sections from 25 IPF, six sarcoidosis and 14 control subjects.COX-1 and COX-2 expression in bronchiolar epithelial cells was significantly lower in IPF and sarcoidosis than in controls. No significant difference was found in COX-2 expression between macrophages in IPF and control sections, but COX-2 was reduced in macrophages in sarcoidosis compared with controls.RESULTSCOX-1 and COX-2 expression in bronchiolar epithelial cells was significantly lower in IPF and sarcoidosis than in controls. No significant difference was found in COX-2 expression between macrophages in IPF and control sections, but COX-2 was reduced in macrophages in sarcoidosis compared with controls.These studies confirm COX-2 loss in bronchial epithelial cells but not macrophages in IPF, and show for the first time reduced constitutive COX-1 expression in epithelial cells and macrophages. Similar abnormalities were observed in sarcoidosis.CONCLUSIONSThese studies confirm COX-2 loss in bronchial epithelial cells but not macrophages in IPF, and show for the first time reduced constitutive COX-1 expression in epithelial cells and macrophages. Similar abnormalities were observed in sarcoidosis. Aims: To test the hypothesis that cyclooxygenase (COX)‐1 or COX‐2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglandin E 2 (PGE 2 ) regulates collagen deposition and fibroblast proliferation and a defect in COX regulation may contribute to the fibrosis that occurs in IPF. Methods: Immunohistochemistry was utilized to determine COX immunoreactivity in lung sections from 25 IPF, six sarcoidosis and 14 control subjects. Results: COX‐1 and COX‐2 expression in bronchiolar epithelial cells was significantly lower in IPF and sarcoidosis than in controls. No significant difference was found in COX‐2 expression between macrophages in IPF and control sections, but COX‐2 was reduced in macrophages in sarcoidosis compared with controls. Conclusions: These studies confirm COX‐2 loss in bronchial epithelial cells but not macrophages in IPF, and show for the first time reduced constitutive COX‐1 expression in epithelial cells and macrophages. Similar abnormalities were observed in sarcoidosis. To test the hypothesis that cyclooxygenase (COX)-1 or COX-2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the cellular distribution. IPF is a progressive inflammatory lung disorder with an adverse prognosis. Previous work has shown that prostaglandin E2 (PGE2) regulates collagen deposition and fibroblast proliferation and a defect in COX regulation may contribute to the fibrosis that occurs in IPF. Immunohistochemistry was utilized to determine COX immunoreactivity in lung sections from 25 IPF, six sarcoidosis and 14 control subjects. COX-1 and COX-2 expression in bronchiolar epithelial cells was significantly lower in IPF and sarcoidosis than in controls. No significant difference was found in COX-2 expression between macrophages in IPF and control sections, but COX-2 was reduced in macrophages in sarcoidosis compared with controls. These studies confirm COX-2 loss in bronchial epithelial cells but not macrophages in IPF, and show for the first time reduced constitutive COX-1 expression in epithelial cells and macrophages. Similar abnormalities were observed in sarcoidosis. |
| Author | Knox, A J Clelland, C A Lewis, S Ronan, J E Petkova, D K |
| Author_xml | – sequence: 1 givenname: D K surname: Petkova fullname: Petkova, D K organization: Respiratory Medicine Unit & Department of Histopathology, University of Nottingham, City Hospital, Nottingham, UK – sequence: 2 givenname: C A surname: Clelland fullname: Clelland, C A organization: Respiratory Medicine Unit & Department of Histopathology, University of Nottingham, City Hospital, Nottingham, UK – sequence: 3 givenname: J E surname: Ronan fullname: Ronan, J E organization: Respiratory Medicine Unit & Department of Histopathology, University of Nottingham, City Hospital, Nottingham, UK – sequence: 4 givenname: S surname: Lewis fullname: Lewis, S organization: Respiratory Medicine Unit & Department of Histopathology, University of Nottingham, City Hospital, Nottingham, UK – sequence: 5 givenname: A J surname: Knox fullname: Knox, A J organization: Respiratory Medicine Unit & Department of Histopathology, University of Nottingham, City Hospital, Nottingham, UK |
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| Keywords | Prostaglandin-endoperoxide synthase Anatomic pathology Pulmonary fibrosis Sarcoidosis Enzyme Systemic disease Idiopathic cyclooxygenase Oxidoreductases idiopathic pulmonary fibrosis immunohistochemistry |
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| Snippet | Aims: To test the hypothesis that cyclooxygenase (COX)‐1 or COX‐2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize... Aims: To test the hypothesis that cyclooxygenase (COX)‐1 or COX‐2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize... To test the hypothesis that cyclooxygenase (COX)-1 or COX-2 expression is defective in lungs in idiopathic pulmonary fibrosis (IPF) and to characterize the... |
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| SubjectTerms | Adult Aged Biological and medical sciences Bronchi - enzymology Bronchi - pathology cyclooxygenase Cyclooxygenase 1 Cyclooxygenase 2 Female Fluorescent Antibody Technique, Indirect Humans idiopathic pulmonary fibrosis immunohistochemistry Investigative techniques, diagnostic techniques (general aspects) Isoenzymes - metabolism Macrophages, Alveolar - enzymology Macrophages, Alveolar - pathology Male Medical sciences Membrane Proteins Middle Aged Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Pneumology Prostaglandin-Endoperoxide Synthases - metabolism Pulmonary Fibrosis - enzymology Pulmonary Fibrosis - pathology Respiratory Mucosa - enzymology Respiratory Mucosa - pathology Respiratory system : syndromes and miscellaneous diseases sarcoidosis Sarcoidosis, Pulmonary - enzymology Sarcoidosis, Pulmonary - pathology Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis |
| Title | Reduced expression of cyclooxygenase (COX) in idiopathic pulmonary fibrosis and sarcoidosis |
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