Anti-neutrophil extracellular trap antibody in a patient with relapse of
anti-neutrophil cytoplasmic antibody-associated vasculitis: a case report
#MMPMID29929470
Shida H
; Hashimoto N
; Kusunoki Y
; Hattanda F
; Ogawa Y
; Hayashi T
; Nakazawa D
; Masuda S
; Tomaru U
; Ishizu A
BMC Nephrol
2018[Jun]; 19
(1
): 145
PMID29929470
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BACKGROUND: Neutrophil extracellular traps (NETs) are web-like DNA decorated with
antimicrobial proteins, such as myeloperoxidase (MPO), which are extruded from
activated neutrophils. Although NETs are essential in innate immunity, an
excessive formation of NETs has adverse effects, e.g., induction of
anti-neutrophil cytoplasmic antibody (ANCA), to the hosts. Since ANCA can induce
NET formation in the primed neutrophils, a positive feedback loop can be formed
between NETs and ANCA, which is called "ANCA-NETs vicious cycle." CASE
PRESENTATION: A 79-year-old Japanese woman developed hydralazine-induced
pauci-immune necrotizing crescentic glomerulonephritis with MPO-ANCA. Although
the illness improved after cessation of hydralazine, MPO-ANCA-associated
vasculitis relapsed 16 months later. Remission was achieved 5 months after
beginning of administration of prednisone. In order to determine the involvement
of ANCA-NETs vicious cycle in this patient, we examined NET degradation and
induction activities in sera obtained at the disease onset (Serum A; MPO-ANCA,
107 IU/ml), at relapse (Serum B; MPO-ANCA, 195 IU/ml), at 3 months after
treatment (Serum C; MPO-ANCA, 4.5 IU/ml), and at remission (Serum D; MPO-ANCA,
2.4 IU/ml). NET degradation activity was low in the all sera. NET induction
activity was high in Sera A, B, and C but not in D. Additionally, we demonstrated
the presence of anti-NET antibody (ANETA) in Sera B and C but not in A or D.
CONCLUSIONS: The collective findings suggest NET induction potential of ANETA in
the present patient and that the ANETA could contribute to the enhancement of
NETs resulting in amplification of the ANCA-NETs vicious cycle.
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