Comparison of two techniques (flow cytometry and alkaline immunophosphatase) in the evaluation of alveolar macrophage immunophenotype

Pérez-Arellano, José-Luis; Losa‐Garcia, J. E.; Orfao‐Matos, A.; González, Manuel A.; Cruz, J. L.; Jiménez, Antonio J.; Castro, S. de

doi:10.1002/dc.2840090304

Cited by 13 publications

(7 citation statements)

References 13 publications

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“…No reaction was observed with anti‐FXIII‐B IgG (not shown). It has been described that bronchoalveolar macrophages contain significantly less CD14 than blood monocytes [25,26] which is consistent with their relatively low labeling intensity for CD14 in our study.…”

Section: Resultssupporting

confidence: 92%

Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation

Katona

Nagy

Kappelmayer

et al. 2005

Journal of Thrombosis and Haemostasis

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In the BALF of controls a low amount of the cellular form of FXIII (FXIII A2) and D-dimer were measured, while plasma FXIII (FXIII A2B2) was absent. Alveolar macrophages represented the single cell population in BALF that contained FXIII. In the BALF of both patients' groups the concentration and the total amount of FXIII A2 was significantly elevated, and plasma FXIII also appeared in the BALF of most patients. The D-dimer concentration was also elevated in the patients' groups and it correlated both with plasma FXIII and neutrophil count. These findings suggest that FXIII A2 is released from activated or injured alveolar macrophages into the bronchoalveolar lining fluid and in bronchoalveolar inflammatory diseases, FXIII A2B2 also leaks out from the capillaries. By cross-linking fibrin and inhibitors of fibrinolysis to fibrin, FXIII might be a key regulator of fibrin turnover in the extravascular compartment.

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Section: Resultssupporting

confidence: 92%

Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation

Katona

Nagy

Kappelmayer

et al. 2005

Journal of Thrombosis and Haemostasis

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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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“…Haslam et al 40 reported an increase in transferrin receptor expression in granulomatous pulmonary disease, although there was considerable within-group variability (14–96%). In contrast, our group found a decreased transferrin receptor expression by the alveolar macrophages of patients with hypersensitivity pneumonitis,41 an observation similar to those of Costabel et al 42…”

Section: Iron Metabolism and The Alveolar Macrophagesupporting

confidence: 87%

Iron metabolism in the lower respiratory tract

Mateos

Brock

Pérez-Arellano

1998

Thorax

147

108

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Comparison of two techniques (flow cytometry and alkaline immunophosphatase) in the evaluation of alveolar macrophage immunophenotype

Cited by 13 publications

References 13 publications

Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation

Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation

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

Iron metabolism in the lower respiratory tract

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