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Vol. 141, No. 1, 2006   

Free Abstract     Article (Fulltext)     Article (PDF 394 KB)     

Original Paper

Investigations on the Involvement of the Lectin Pathway of Complement Activation in Anaphylaxis
Michaela Windbichlera, Bernd Echtenachera, Kazue Takahashic, R. Alan B. Ezekowitzc, Wilhelm J. Schwaebleb, Jens C. Jenseniuisd, Daniela N. Männela

aInstitute of Immunology, University of Regensburg, Regensburg, Germany;
bDepartment of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK;
cDepartment of Pediatrics, Laboratory of Developmental Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Mass., USA;
dDepartment of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark

Address of Corresponding Author

Int Arch Allergy Immunol 2006;141:11-23 (DOI: 10.1159/000094177)


 goto top of page Key Words

  • Mannan-binding lectin
  • Mast cells
  • Anaphylactic shock
  • Proteoglycans
  • Chondroitin sulphate

 goto top of page Abstract

Background: Systemic anaphylaxis is the most severe form of immediate hypersensitivity reaction. The activation of the complement system occurs during anaphylactic shock. The purpose of this study was to determine in a mouse model whether the lectin pathway of complement activation is involved in anaphylaxis. Methods: To see whether the lectin pathway is involved in anaphylactic shock, serum mannan-binding lectin (MBL) levels were measured after passive anaphylaxis. Also MBL expression and binding to potential ligands were investigated. To determine whether complement or mast cell activation is essential for hypothermia in anaphylactic shock, mouse strains deficient in MBL-A and MBL-C, C1q, factors B and C2, C5, C5aR, or mast cells were tested. Results: After antigenic challenge a marked drop in body temperature as well as a rapid decrease in serum MBL levels were observed. The decrease of serum MBL levels in shock could not be attributed to MBL binding to immune complexes or tissues, but an interaction of MBL with mast cell-derived proteoglycans was seen. In contrast to mast cell-deficient mice, none of the complement-deficient mouse strains were protected from shock-associated hypothermia. Conclusions: These results indicate that neither MBL nor activation of the complement cascade is crucial for the induction of anaphylaxis. In contrast mast cell activation is associated with the development of hypothermia and possibly the observed decrease in serum MBL levels.

Copyright © 2006 S. Karger AG, Basel


 goto top of page Author Contacts

Correspondence to: Dr. Daniela N. Männel
Institute of Immunology, University of Regensburg
F.-J.-Strauss-Allee 11, DE-93042 Regensburg (Germany)
Tel. +49 941 944 6622, Fax +49 941 944 6602 E-Mail daniela.maennel@klinik.uni-regensburg.de


 goto top of page Article Information

Received: November 10, 2005
Accepted after revision: February 27, 2006
Published online: June 23, 2006
Number of Print Pages : 13
Number of Figures : 7, Number of Tables : 0, Number of References : 49

 
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Medline Abstract (ID 16804320)
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