Abstract：
:The aim of this study was to determine the contribution of neutrophils to adjuvant arthritis (AA) by in vivo depletion of peripheral blood neutrophils. Specific anti-neutrophil MoAb, RP3 (10 mg), or a control antibody was given twice daily on days 8-11 after injection of Mycobacterium tuberculosis in inbred male Sprague-Dawley rats. RP3 treatment inhibited the neutrophil leukocytosis associated with AA (3.3 +/- 0.6 x 10(3)/mm3 versus 21.2 +/- 6.9 x 10(3)/mm3; P<0.001). On day 12, control animals exhibited severe arthritis as assessed by articular index (AI) (9.2 +/- 1.3), increase in paw volume (149.3 +/- 10.6%), and synovial fluid (SF) cell count (5.3 +/- 0.5 x 10(5)). RP3 treatment significantly reduced AI (1 +/- 0.1; P<0.001), paw volume (103.6 +/- 5.8%; P<0.001) and SF cells (0.6 +/- 0.1 x 10(5); P<0.001) without affecting cutaneous DTH (treated 0.6 +/- 0.1 mm change in thickness, control 0.8 +/- 0.2 mm; NS). Additional experiments demonstrated that CD4+ cell depletion but not decomplementation inhibited AA development and synovial neutrophil accumulation. Depletion of circulating neutrophils prevented joint inflammation and synovial leucocyte influx in AA, suggesting a pivotal role for neutrophils in the effector phase of AA. Inhibition of neutrophil accumulation by CD4+ cell depletion and not by decomplementation suggests that neutrophil accumulation in AA is T cell-dependent.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Santos LL,Morand EF,Hutchinson P,Boyce NW,Holdsworth SRdoi
10.1111/j.1365-2249.1997.263-ce1154.xsubject
Has Abstractpub_date
1997-02-01 00:00:00pages
248-53issue
2eissn
0009-9104issn
1365-2249journal_volume
107pub_type
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