Phagocytosis of Agarose Beads by Receptors for C3b (CR1) and iC3b (CR3) on Alveolar Macrophages from Patients with Sarcoidosis

Pettersen, H. B.; Johnson, Egil; Osen, S. S.

doi:10.1111/j.1365-3083.1990.tb03209.x

Cited by 13 publications

(9 citation statements)

References 27 publications

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“…It has been shown that the C3bi-mediated phagocytosis of agarose beads is dependent on CD1 lb [105]. The enhanced respiratory burst of the alveolar macrophages seen in sarcoidosis also depends on the expression of CDll/CD18 epitopes [115].…”

Section: Sarcoidosismentioning

confidence: 99%

Adhesion molecules in lung diseases

Hamacher¹,

Schaberg²

1994

Lung

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The human body possesses highly specialized cellular defense mechanisms that, when activated pathologically, can induce a number of immunologic disorders. For a normal cellular immune response, the following conditions must be fulfilled: (1) accumulation of white blood cells, (2) their diapedesis through the vessel walls of the inflammatory area affected by an injurious agent, and (3) normal cellular effector functions in the tissue. This cascade of inflammatory processes has recently been shown to be regulated by a group of molecules that are termed adhesion molecules and consist of three subfamilies: selectins, the immunoglobulin supergene family, and integrins. The cellular functions influenced by adhesion molecules include, among others, cytotoxic T-cell responses, CD4-dependent activation of B lymphocytes by T lymphocytes, activation of granulocytes and macrophages, phagocytosis of opsonized particles by monocytes, macrophages, and granulocytes, antigen-presenting function of macrophages, their antibody-dependent cytotoxicity, initiation of a respiratory burst by white blood cells, and activation of fibroblasts. Studies performed in recent years have shown that pathogenetically relevant changes in the expression and function of adhesion molecules are involved in a variety of pulmonary diseases. These changes include the accumulation and activation of alveolar macrophages in smokers, experimentally induced bronchial hyperreactivity in bronchial asthma, accumulation of eosinophils in allergic rhinitis, bleomycin-induced pulmonary fibrosis, binding of viruses and bacteria to respiratory mucosa, and various mechanisms of acute damage to pulmonary parenchyma. Though their role in tumor development is still unclear, adhesion molecules are obviously involved in determining the route and organotropism of metastases. Further studies of the function of adhesion molecules in pulmonary diseases will contribute to our understanding of the pathomechanisms of these diseases and, through the development of specific antibodies, may provide attractive new therapeutic approaches to problems for which treatment is not yet available.

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Section: Sarcoidosismentioning

confidence: 99%

Adhesion molecules in lung diseases

Hamacher¹,

Schaberg²

1994

Lung

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“…Increases of C3a levels in BAL [34] and of complement synthesis by AMs have been observed [19,42]. Compared to normal controls, PET-TERSEN et al [43] found a higher expression of CR1 and CR3 and phagocytosis of AMs in patients with sarcoidosis stages I to III according to SILTZBACH [44]. In sarcoidosis, sCR1 correlated with the BAL lymphocyte count, suggesting a lymphocyte-dependent sCR1 production in this disease.…”

Section: Discussionmentioning

confidence: 93%

Soluble complement receptor type 1 (CD35) in bronchoalveolar lavage of inflammatory lung diseases

Hamacher¹,

Sadallah²,

Ja³

et al. 1998

Eur Respir J

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Complement receptor type 1 (CR1) (CD35; C3b/C4b receptor) is a transmembrane protein of many haematopoietic cells. Once cleaved, soluble complement receptor type 1 (sCR1) exerts opposite effects as a powerful inhibitor of complement. This study addressed both the question of whether sCR1 was found in bronchoalveolar lavage (BAL) of normals and patients with various inflammatory disease, and its possible origin. In this retrospective study covering specimen and clinical data of 124 patients with acute and chronic inflammatory lung pathologies, BAL supernatants were analysed by enzyme-linked immunosorbent assay technique for sCR1. Correlations were made between the sCR1 levels obtained and the constituents of BAL. Human alveolar macrophages were cultivated in order to determine their secretory capacity of sCR1. Alveolar macrophages from normal subjects were shown to release sCR1 in vitro. In addition, sCR1 was present in BAL of normal controls and was significantly increased in acute inflammatory lung diseases such as acute respiratory distress syndrome (ARDS), bacterial and Pneumocystis carinii pneumonia, as well as in chronic inflammatory diseases such as interstitial lung fibrosis and sarcoidosis. In BAL of ARDS, bacterial, and P. carinii pneumonia, there was a good correlation between sCR1 and the absolute neutrophil counts. In sarcoidosis, a correlation was found with BAL lymphocyte counts. Serum sCR1 was not increased in patients compared to controls. Soluble complement receptor type 1 (sCR1) is found in the bronchoalveolar lavage in health as well as in acute and chronic inflammatory disease. Alveolar macrophages are capable of releasing sCR1 in vitro and may be the main physiological source of sCR1 in the alveoli. The good correlation between sCR1 and the absolute neutrophil or lymphocyte numbers in bronchoalveolar lavage of inflammatory diseases suggests a predominant role of leucocytes for the release of sCR1 in such conditions. The release of this inhibitor of complement may be crucial to control and reduce complement activation and thus prevent lung injury.

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“…Furthermore, increased CD lib expression on BAL macrophages is associated with disease activity in sarcoidosis, another frequent ILD [11], Similarly, an increased expression of surface mole cules of the CD11/CD18 family appears to be closely related with an exaggerated production of superoxide anions by these inflammatory cells [12]. Oxidant injury plays an important role in a number of human and experi mental acute and chronic lung disorders [13,14], There fore, the increased expression of CD 11 /CD 18 epitopes on macrophages obtained from injured lungs seems to be accompanied by changes in cell function, and for exam ple, it has been demonstrated that the C3bi-mediated phagocytosis of agarose beads is dependent on C D llb [15].…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Intercellular Adhesion Molecule 1, CD11/CD18 Cell Surface Adhesion Glycoproteins and α4β1 Integrin in a Rat Model of Chronic Interstitial Lung Fibrosis

et al. 1996

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The expression of the intercellular adhesion molecule 1 (ICAM-1), and the integrins CD49, CD1 Vole, and CD1 la (LFA-1α chain) was analyzed in an experimental model of pulmonary fibrosis. Adult rats were exposed to 75% oxygen during 10 weeks, and to 2.0 mg/kg of paraquat twice weekly. Rats were sacrificed at 2 days, and at 2 and 10 weeks after the first injection of paraquat. Lungs were fixed in 4% paraformaldehyde and used for histology and immunohistochemistry. At 2 days the lungs showed a diffuse inflammation composed of a mixed polymorphonuclear and mononuclear cell infiltrate. Afterwards, the inflammatory process was predominantly mononuclear, and an increasing fibroblast proliferation was observed. Early inflammatory events (48 h) correlated with a moderate increased expression of ICAM-1, LFA, and CD1 lb/c in epithelial cells as well as a pronounced expression of ICAM-1 and CD1 lb/c in macrophages. At 2 and 10 weeks, there was a progressive increased expression of CD1 lb/c and ICAM-1 by macrophages, as well as of LFA in epithelial cells, and of ICAM-1 and CD49 by epithelial and interstitial cells. Lymphocytes showed a slight increased expression of LFA at 2 weeks, and of CD49 at 2 and 10 weeks. These results suggest that macrophages expressing ICAM-1, CD1 lb/c, and CD49 are involved in the earlier and late phases of the disease whereas fibroblast and epithelial cells expressing ICAM-1 and CD49 might play a role in the cell interactions involved in the fibrotic phase.

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Phagocytosis of Agarose Beads by Receptors for C3b (CR1) and iC3b (CR3) on Alveolar Macrophages from Patients with Sarcoidosis

Cited by 13 publications

References 27 publications

Adhesion molecules in lung diseases

Adhesion molecules in lung diseases

Soluble complement receptor type 1 (CD35) in bronchoalveolar lavage of inflammatory lung diseases

Increased Expression of Intercellular Adhesion Molecule 1, CD11/CD18 Cell Surface Adhesion Glycoproteins and α4β1 Integrin in a Rat Model of Chronic Interstitial Lung Fibrosis

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Phagocytosis of Agarose Beads by Receptors for C3b (CR1) and iC3b (CR3) on Alveolar Macrophages from Patients with Sarcoidosis

Cited by 13 publications

References 27 publications

Adhesion molecules in lung diseases

Adhesion molecules in lung diseases

Soluble complement receptor type 1 (CD35) in bronchoalveolar lavage of inflammatory lung diseases

Increased Expression of Intercellular Adhesion Molecule 1, CD11/CD18 Cell Surface Adhesion Glycoproteins and &alpha;4&beta;1 Integrin in a Rat Model of Chronic Interstitial Lung Fibrosis

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Increased Expression of Intercellular Adhesion Molecule 1, CD11/CD18 Cell Surface Adhesion Glycoproteins and α4β1 Integrin in a Rat Model of Chronic Interstitial Lung Fibrosis