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

E. Katona, B. Nagy, J. Kappelmayer, G. Baktai, L. Kovács, T. Márialigeti, B. Dezső, L. Muszbek

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Extravascular activation of the coagulation system and consequent fibrin deposition is involved in the pathomechanism of chronic bronchoalveolar inflammatory diseases. The turnover of extra vascular 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 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 A 2B2 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 extra vascular compartment.

Original languageEnglish
Pages (from-to)1407-1413
Number of pages7
JournalJournal of Thrombosis and Haemostasis
Volume3
Issue number7
DOIs
Publication statusPublished - 2005

Fingerprint

Factor XIII
Bronchoalveolar Lavage Fluid
Inflammation
Fibrin
varespladib methyl
Alveolar Macrophages
Blood Vessels
Factor XIIIa
Bronchitis
Pulmonary Fibrosis
Fibrinolysis
Immunoassay

Keywords

  • Bronchoalveolar inflammation
  • Bronchoalveolar lavage fluid
  • Factor XIII

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation. / Katona, E.; Nagy, B.; Kappelmayer, J.; Baktai, G.; Kovács, L.; Márialigeti, T.; Dezső, B.; Muszbek, L.

In: Journal of Thrombosis and Haemostasis, Vol. 3, No. 7, 2005, p. 1407-1413.

Research output: Contribution to journalArticle

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abstract = "Background: Extravascular activation of the coagulation system and consequent fibrin deposition is involved in the pathomechanism of chronic bronchoalveolar inflammatory diseases. The turnover of extra vascular 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 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 A 2B2 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 extra vascular compartment.",
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T1 - Factor XIII in bronchoalveolar lavage fluid from children with chronic bronchoalveolar inflammation

AU - Katona, E.

AU - Nagy, B.

AU - Kappelmayer, J.

AU - Baktai, G.

AU - Kovács, L.

AU - Márialigeti, T.

AU - Dezső, B.

AU - Muszbek, L.

PY - 2005

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N2 - Background: Extravascular activation of the coagulation system and consequent fibrin deposition is involved in the pathomechanism of chronic bronchoalveolar inflammatory diseases. The turnover of extra vascular 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 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 A 2B2 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 extra vascular compartment.

AB - Background: Extravascular activation of the coagulation system and consequent fibrin deposition is involved in the pathomechanism of chronic bronchoalveolar inflammatory diseases. The turnover of extra vascular 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 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 A 2B2 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 extra vascular compartment.

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KW - Bronchoalveolar lavage fluid

KW - Factor XIII

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