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Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation
Author(s) -
KATONA É.,
NAGY B.,
KAPPELMAYER J.,
BAKTAI G.,
KOVÁCS L.,
MÁRIALIGETI T.,
DEZS? B.,
MUSZBEK L.
Publication year - 2005
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2005.01353.x
Subject(s) - bronchoalveolar lavage , fibrin , factor xiii , immunology , medicine , inflammation , coagulation , fibrinolysis , fibrinogen , lung , population , pathology , environmental health
Summary. Background: Extravascular activation of the coagulation system and consequent fibrin deposition is involved in the pathomechanism of chronic bronchoalveolar inflammatory diseases. The turnover of extravascular fibrin is attenuated by its cross‐linking with activated factor XIII (FXIII). Objectives: Determination of cellular and plasmatic forms of FXIII and their correlation with D‐dimer level in the bronchoalveolar lavage fluid (BALF) from healthy children and from children with bronchoalveolar inflammation. Patients and methods: Highly sensitive immunoassays were used for the quantitation of cellular and plasma FXIII and D‐dimer in the BALF of children with recurrent wheezy bronchitis and fibrosing alveolitis. BALF was investigated for FXIII‐containing cells by flow cytometry. Results and conclusions: In the BALF of controls a low amount of the cellular form of FXIII (FXIII A 2 ) and D‐dimer were measured, while plasma FXIII (FXIII A 2 B 2 ) 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 A 2 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 A 2 is released from activated or injured alveolar macrophages into the bronchoalveolar lining fluid and in bronchoalveolar inflammatory diseases, FXIII A 2 B 2 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.