Pulmonary haptoglobin and CD163 are functional immunoregulatory elements in the human lung
1Clinical and Experimental Pathology, Research Center Borstel, Borstel, Germany.
Respiration; International Review of Thoracic Diseases
|August 24, 2011
Summary
Pulmonary haptoglobin (pHp) and its receptor CD163 are expressed in the human lung, playing a role in immune defense during respiratory infections and inflammation. Their local regulation and secretion contribute to the respiratory system's inflammatory response.
Area of Science:
- Pulmonary immunology
- Molecular biology
- Cellular biology
Background:
- Haptoglobin (Hp) and its receptor CD163 are known immunomodulators with anti-inflammatory and antioxidant functions.
- Pulmonary Hp (pHp) and CD163 roles in lung inflammation and infection require further elucidation.
Purpose of the Study:
- Investigate the expression, regulation, and secretion of pulmonary Hp (pHp) and CD163 in the human lung.
- Determine the cellular events and mediator release upon stimulation with inflammatory stimuli and respiratory pathogens.
- Assess pHp and CD163 expression in Chronic Obstructive Pulmonary Disease (COPD) and sarcoidosis.
Main Methods:
- Utilized a human ex vivo lung tissue culture model and A549/alveolar epithelial cell type II cultures.
- Employed immunohistochemistry, immunocytochemistry, in situ hybridization, immunofluorescence, and various PCR techniques.
- Performed Western immunoblot, ELISA, and cytometric bead array analyses on tissue lysates and supernatants.
Main Results:
- Demonstrated the expression, regulation, and secretion of pHp and CD163 in the human lung for the first time.
- Observed the release of soluble mediators and chemoattractants from A549 cells and macrophages upon Hp stimulation.
- Indicated differential activation of mediator release by Hp.
Conclusions:
- pHp and CD163 function as pulmonary defense elements in the human lung.
- Local expression, regulation, and secretion are key to their role during lung infection.
- These molecules are integral to the inflammatory immune response of the respiratory system.
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