Fig. 6From: Therapeutic blockade of HMGB1 reduces early motor deficits, but not survival in the SOD1G93A mouse model of amyotrophic lateral sclerosisImmune and inflammatory markers are not altered in tibialis anterior and gastrocnemius muscle of anti-HMGB1 antibody-treated SOD1G93A mice. SOD1G93A mice were intraperitoneally injected weekly with the anti-HMGB1 antibody at 35 days of age (100 μg). Pro-inflammatory cytokines (TNFα and IL-1β) and major innate immune receptors (RAGE, C5aR1 and TLR4) in tibialis anterior (TA) and gastrocnemius (GN) muscle of vehicle and anti-HMGB1-treated SOD1G93A mice was investigated at mid-symptomatic stage of disease (133 days) using quantitative PCR. a, b Shows no change in pro-inflammatory cytokines Tnf and Il1β in both TA and GN muscle of anti-HMGB1-treated SOD1G93A mice when compared to isotype control-treated SOD1G93A mice (n = 6, p > 0.05, Student’s t test). Ager and C5ar1 mRNA transcript levels were not different in isotype control and anti-HMGB1-treated SOD1G93A mice in both TA and GN muscle (c, d; n = 6, p > 0.05, Student’s t test). While anti-HMGB1 treatment showed a slight reduction in Tlr4 transcript levels in TA muscle, no change was observed in GN muscle of SOD1G93A mice (e; n = 6 *p < 0.05, Student’s t test). Data are presented as mean ± SEMBack to article page