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* Cytokine Research Unit and the
Inflammation Research Unit, School of Pathology, The University of New South Wales, Kensington 2052, Australia
Correspondence: Carolyn L. Geczy, Cytokine Research Unit, School of Pathology, The University of New South Wales, Kensington, New South Wales 2052, Australia. E-mail: C.Geczy{at}unsw.edu.au
S100 proteins represent a new class of chemoattractants. Here we extend
earlier evidence for the proinflammatory properties of human S100A12.
A12 induced migration of monocytoid cells, with optimal activity at
10-10 M and potency of >10-9 M C5a.
Neutrophils were poorly responsive, and lymphocyte migration was not
affected. Actin polymerization in monocytoid cells was accompanied by a
sustained [Ca2+]i flux of a magnitude
comparable with C5a. A12 elicited a transient infiltration of
neutrophils (4–8 h) and more delayed recruitment of monocytes (8–24
h) in vivo. A12 (
70 nM) was present in synovial fluid (SF) from
rheumatoid arthritis patients, and synovium contained A12-positive
neutrophils in the sublining and interstitial region, often surrounding
the perivasculature but rarely in the synovial lining layer, although
some macrophages were positive. The A12 gene was transiently
up-regulated in monocytes by tumor necrosis factor 
(6 h); induction
by lipopolysaccharide (LPS) was sustained (12–48 h). A12 may
contribute to leukocyte migration in chronic inflammatory
responses.
Key Words: leukocyte recruitment • rheumatoid arthritis • gene induction
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