Differences in expression of monocyte/macrophage surface antigens in peripheral blood and bronchoalveolar lavage cells in interstitial lung diseases

Hoogsteden, Henk C.; Hal, Peter Th. W. van; Wijkhuijs, J M; Hop, W. C. J.; Hilvering, C

doi:10.1007/bf00183944

Cited by 18 publications

(15 citation statements)

References 29 publications

(20 reference statements)

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“…CD14, a surface marker for both monocytes and macrophages, was dramatically down‐regulated during culture. With regard to lung macrophages, this observation is in accordance with the findings of other groups (Perez‐Arellano et al , 1993; Hoogsteden et al , 1993), and supports the view that under our culture conditions macrophages of an alveolar type may arise. Importantly, the myeloid markers CD45 and CD13 remained stable, and the monocyte‐derived cells were devoid of any CD1a expression.…”

Section: Discussionsupporting

confidence: 93%

In vitro differentiation of human monocytes to macrophages: change of PDE profile and its relationship to suppression of tumour necrosis factor‐α release by PDE inhibitors

Gantner

Kupferschmidt

Schudt

et al. 1997

British J Pharmacology

133

107

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1 During in vitro culture in 10% human AB serum, human peripheral blood monocytes acquire a macrophage-like phenotype. The underlying di erentiation was characterized by increased activities of the macrophage marker enzymes unspeci®c esterase (NaF-insensitive form) and acid phosphatase, as well as by a down-regulation in surface CD14 expression. 2 In parallel, a dramatic change in the phosphodiesterase (PDE) pro®le became evident within a few days that strongly resembled that previously described for human alveolar macrophages. Whereas PDE1 and PDE3 activities were augmented, PDE4 activity, which represented the major cyclic AMPhydrolysing activity of peripheral blood monocytes, rapidly declined. 3 Monocytes and monocyte-derived macrophages responded to lipopolysaccharide (LPS) with the release of tumour necrosis factor-a (TNF). In line with the change in CD14 expression, the EC 50 value of LPS for induction of TNF release increased from approximately 0.1 ng ml 71 in peripheral blood monocytes to about 2 ng ml 71 in macrophages. 4 Both populations of cells were equally susceptible towards inhibition of TNF release by cyclic AMP elevating agents such as dibutyryl cyclic AMP, prostaglandin E 2 (PGE 2 ) or forskolin, which all led to a complete abrogation of TNF production in a concentration-dependent manner and which were more e cient than the glucocorticoid dexamethasone. 5 In monocytes, PDE4 selective inhibitors (rolipram, RP73401) suppressed TNF formation by 80%, whereas motapizone, a PDE3 selective compound, exerted a comparatively weak e ect (10 ± 15% inhibition). Combined use of PDE3 plus PDE4 inhibitors resulted in an additive e ect and fully abrogated LPS-induced TNF release as did the mixed PDE3/4 inhibitor tolafentrine. 6 In monocyte-derived macrophages, neither PDE3-nor PDE4-selective drugs markedly a ected TNF generation when used alone (515% inhibition), whereas in combination, they led to a maximal inhibition of TNF formation by about 40 ± 50%. However, in the presence of PGE 2 (10 nM), motapizone and rolipram or RP73401 were equally e ective and blocked TNF release by 40%. Tolafentrine or motapizone in the presence of either PDE4 inhibitor, completely abrogated TNF formation in the presence of PGE 2 . Thus, an additional cyclic AMP trigger is necessary for PDE inhibitors to become e ective in macrophages. 7 Finally, the putative regulatory role for PDE1 in the regulation of TNF production in macrophages was investigated. Zaprinast, at a concentration showing 80% inhibition of PDE1 activity (100 mmol l 71 ), did not in¯uence TNF release. At higher concentrations (1 mmol l 71 ), zaprinast became e ective, but this inhibition of TNF release can be attributed to a signi®cant inhibitory action of this drug on PDE3 and PDE4 isoenzymes. 8 In summary, the in vitro di erentiation of human peripheral blood monocytes to macrophages is characterized by a profound change in the PDE isoenzyme pattern. The change in the PDE4 to PDE3 ratio is functionally re¯ected by an altered susceptibility towards selective PDE ...

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Section: Discussionsupporting

confidence: 93%

In vitro differentiation of human monocytes to macrophages: change of PDE profile and its relationship to suppression of tumour necrosis factor‐α release by PDE inhibitors

Gantner

Kupferschmidt

Schudt

et al. 1997

British J Pharmacology

133

107

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“…Increased expression of CD13 has previously been reported in ILD patients (14) and tissue macrophages from patients with idiopathic retroperitoneal fibrosis (17). Other markers of varying functions such as CD9, CD52, CD71, and HLA Class I were expressed at higher levels in ILD patients.…”

Section: Phenotype Of Alveolar Macrophages In Ildmentioning

confidence: 89%

Extensive Surface Phenotyping of Alveolar Macrophages in Interstitial Lung Disease

Taylor

Noble

White

et al. 2000

Clinical Immunology

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“…In favour of local production are experiments showing upregulation of CD14 expression in pulmonary diseases characterized by chronic alveolar macrophage activation [21,22]. Using radioisotope flux studies in interstitial lung disease, the authors have suggested that elevated BAL albumin levels are related to local inflammation, rather than acute permeability changes due to the BAL procedure itself [18].…”

Section: Discussionmentioning

confidence: 99%

Increased soluble CD14 in bronchoalveolar lavage fluid of stable lung transplant recipients

et al. 2002

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Macrophages, neutrophils and infection have been implicated in the genesis of the bronchiolitis obliterans syndrome (BOS) post lung transplantation. sCD14 is a soluble form of a shed-cell surface protein. It is capable of promoting cytokine-induced inflammation and it9s presence in clinically stable lung transplant recipients (LTR) might be important as an early marker of BOS.Bronchalveolar lavage (BAL) and blood samples were taken from 26 stable LTR, at or near their best forced expiratory volume in one second who were free from infection. sCD14 levels were measured via enzyme-linked immunosorbent assay. Cell counts were performed on unfiltered BAL.LTR neutrophil count, BAL sCD14 and serum sCD14 levels were higher than controls (median 3.8% versus 1.3%, pv0.05; 11.5 ng?mL -1 versus 6 ng?mL -1 , pv0.001; 6.2 mg?mL -1 versus 2.4 mg?mL -1 , pv0.05, respectively). BAL albumin and sCD14 correlated (regression coefficient: 0.77, pv0.001).In this hypothesis-generating, cross-sectional study, the authors have described for the first time soluble CD14 levels in the bronchoalveolar lavage and serum of stable lung transplant recipients, and show that these are elevated compared to controls. This is a practicable candidate marker system, which can be tested for a predictive role in bronchiolitis obliterans syndrome following lung transplantation. The origin of this cellular protein and its temporal relationship to the development of the bronchiolitis obliterans syndrome remains to be elucidated in more definitive longitudinal studies, which should include other measurements potentially relevant to the innate immune system, such as bronchoalveolar lavage endotoxin levels.

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Differences in expression of monocyte/macrophage surface antigens in peripheral blood and bronchoalveolar lavage cells in interstitial lung diseases

Cited by 18 publications

References 29 publications

In vitro differentiation of human monocytes to macrophages: change of PDE profile and its relationship to suppression of tumour necrosis factor‐α release by PDE inhibitors

In vitro differentiation of human monocytes to macrophages: change of PDE profile and its relationship to suppression of tumour necrosis factor‐α release by PDE inhibitors

Extensive Surface Phenotyping of Alveolar Macrophages in Interstitial Lung Disease

Increased soluble CD14 in bronchoalveolar lavage fluid of stable lung transplant recipients

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