Cytokine production profile of splenocytes derived from zymosan A-treated SKG mice developing arthritis

• Published in: Inflammation research Vol. 55; no. 8; pp. 335 - 341
• Main Authors: Kobayashi, K, Suda, T, Nan-Ya, K, Sakaguchi, N, Sakaguchi, S, Miki, I
• Format: Journal Article
• Language: English
• Published: Switzerland Springer Nature B.V 01.08.2006
• Subjects: Animals; Arthritis - metabolism; Arthritis, Experimental - pathology; Cytokines - biosynthesis; Disease Models, Animal; Interleukin-2 - metabolism; Interleukin-4 - metabolism; Interleukin-6 - metabolism; Mice; Mice, Inbred BALB C; Species Specificity; Spleen - metabolism; T-Lymphocytes - metabolism; Th2 Cells - metabolism; Zymosan - pharmacology
• ISSN: 1023-3830; 1420-908X
• DOI: 10.1007/s00011-006-5208-x

SKG mice have a point mutation of the zeta-associated protein of 70 kD (ZAP-70) and spontaneously develop a severe polyarthritis in the conventional condition, whereas they are healthy under the specific pathogen free (SPF) condition. The purpose of this study was to investigate the cytokine production from splenocytes in SKG mice developing arthritis under the SPF condition. SKG and BALB/c mice were intraperitoneally injected with zymosan A under the SPF condition. Spleen was isolated 1, 2 or 8 weeks after the intraperitoneal injection of saline or zymosan A. Splenocytes were cultured with concanavalin A. Cytokine production and proliferation were measured 48 and 72 h after the culture. An intraperitoneal injection of zymosan A induced severe polyarthritis with increased levels of rheumatoid factor and interleukin 6 (IL-6) only in SKG mice. Splenocytes from SKG mice did not proliferate well maybe because of less productivity of IL-2. The IL-4 production from splenocytes of SKG mice was higher, while interferon-gamma production was lower than those of BALB/c mice. An injection of zymosan A reduced the IL-4 production only in SKG mice. SKG mice do not develop arthritis under the SPF condition possibly because of a low proliferative activity of T cells and Th2-predominance.