Increased neutrophil apoptosis during attacks of familial Mediterranean fever

Citation
S. Ozen et al., Increased neutrophil apoptosis during attacks of familial Mediterranean fever, CLIN EXP RH, 19(5), 2001, pp. S68-S71
Citations number
10
Categorie Soggetti
Rheumatology,"da verificare
Journal title
CLINICAL AND EXPERIMENTAL RHEUMATOLOGY
ISSN journal
0392856X → ACNP
Volume
19
Issue
5
Year of publication
2001
Supplement
24
Pages
S68 - S71
Database
ISI
SICI code
0392-856X(200109/10)19:5<S68:INADAO>2.0.ZU;2-9
Abstract
Aim Apoptosis is a programmed form of cell death. Recently much attention h as been devoted to the role of apoptosis in rheumatological diseases. We ha ve aimed to analyze apoptosis in the inflammatory pathway of familial Medit erranean fever (FMF). Methods 26 FMF patients and 12 age and sex matched controls were the subjec t of the study. Twelve of the patients were analyzed during an FMF attack w hereas samples were obtained at least a week after an attack in 14. Four of the patients had renal amyloidosis. Whole blood was treated with ammonium chloride for RBC lysis. Subsequently the cells were stained with propidium iodide and annexin. Neutrophils and lymphocytes were gated separately for a nalysis by flow cytometry. We have also analyzed cellular Fas and Fas-ligan d expression in these cells. Results The mean age of the patients was 12.00 +/- 3.17, and was not differ ent than the control subjects. Erythrocyte sedimentation rate and CRP level s were significantly elevated in the attack group as compared to the attack -free group. The mean levels of neutrophil apoptosis in the FMF patients wi th an attack, attack-free and controls were 12.94 +/- 11.78, 6.60 +/- 7.83 and 3.98 +/- 4.27, respectively. Lymphocyte apoptosis in the same groups we re 7.84 +/- 8.63, 2.75 +/- 2.33, and 1.22 +/- 0.93, respectively. Neutrophi l and monocyte apoptosis was significantly increased during the attack as c ompared to the controls (p < 0.05). However lymphocyte apoptosis was not di fferent between the aforementioned groups. On the other hand, lymphocyte ap optosis was significantly increased in the SLE patients (p < 0.05), whereas neutrophil apoptosis was not, Fas staining of neutrophils were not differe nt between the groups (p > 0.05). On the other hand the difference between the groups for FasL was significant (p < 0.05) Conclusion Neutrophil and monocyte but not lymphocyte apoptosis was signifi cantly increased during FMF attacks reminding us that FMF is an autoinflamm ation of certain peripheral cells. The increased apoptosis in these patient s maybe regarded as a response to clear the unwanted inflammatory cells. On the other hand the increased apoptosis maybe the explanation of the self-l imited nature of the FMF attacks. Future studies will enlighten us on the s ignificance of this increased apoptosis in the process of inflammation.