s32_ab15

ANCA against bactericidal/permeability-increasing protein, azurocidin, calprotectin and defensins in rheumatic and infectious diseases: Prevalence and clinical associations

H. Schultz*, E. Csernok*, K. Herlyn, P.H. Reichel, F. Moosig, O.A. Cornely¹, M.K. Fagerhol², W.L. Gross

Department of Rheumatology, University of Lübeck, Lübeck and Rheumaklinik Bad Bramstedt GmbH, Bad Bramstedt, Germany; ¹Department of Internal Medicine I, Hematology - Oncology, Infectious Diseases and Rheumatology, University of Cologne, Germany; ²Blood Bank and Department of Immunology, Ulleval Hospital, Oslo, Norway.

ABSTRACT
Objective
To determine the prevalence and clinical associations of ANCA against the antibiotic proteins and peptides: Bactericidal/permeability-increasing protein (BPI), Azurocidin (AZ), Calprotectin (CP) and b-Defensin-1 and -2 (DF).

Methods
Patients with ANCA-associated vasculitides (n = 99), other vasculitides and rheumatic connective tissue diseases (n = 303), HIV-infection (n = 66), other infectious diseases (n = 134) Crohn's disease (n = 12) and ulcerative colitis (n = 12) were tested for BPI-, AZ-, CP-, DF-, PR3-, and MPO-ANCA in indirect immunofluorescence technique (IFT) and ELISA.

Results
In ANCA associated vasculitides BPI-ANCA were detected in 6% of patients. In HIV infection, BPI was the main target antigen of ANCA-IFT positive sera (74%). BPI-ANCA was associated with higher inflammatory activity. In Crohn's disease and ulcerative colitis BPI-ANCA was prominent (34% of patients). AZ-ANCA were found in 5% of patients. No ANCA were detected against defensin and calprotectin.

Conclusion
BPI-ANCA is the main autoantibody in HIV and is associated with higher inflammatory activity. In inflammatory bowel diseases BPI-ANCA is predominant, AZ-ANCA are also present to a lesser extend. Both were not useful characterize clinical subgroups. No ANCA were detected against calprotectin or defensins.

Key words
ANCA , infectious diseases, bactericidal/permeability increasing protein, ELISA, indirect immunofluorescence technique, HIV.

*Both of these authors contributed equally to this publication.
This work was supported by DFG Grant Schu 1308/1-1 (to H.S.), and grants from the Forschungsschwerpunkt 'Koerpereigene Infektabwehr' of the University of Lübeck (to H.S.) and the Kompetenznetz-werk Rheuma (to E.C. and H.S.).
Please address correspondence and reprint requests to: Elena Csernok, PhD, Rheumaklinik Bad Bramstedt GmbH, P.O. Box 1448, D-24572 Bad Bramstedt, Germany.