Human C-Reactive Protein [His]

The objective of this study is to compare the effects of virtual reality training (VRT) and sensory-motor training (SMT) in bone morphogenetic proteins (BMP) and inflammatory biomarkers expression in post-traumatic osteoarthritis (PTOA) after the anterior cruciate ligament injury. Through a simple random sampling method, 60 eligible participants were allocated into VRT (n = 20), SMT (n = 20), and control groups (n = 20). They underwent training programs for 4 weeks. Clinical (pain intensity and functional disability) and biochemical (bone morphogenic proteins and inflammatory biomarkers) values were measured at baseline, after 4 weeks, 8 weeks and 3 months follow up. Four weeks following training, the VRT group shows more significant changes in pain intensity and functional disability than SMT and control groups (P < 0.001). Bone morphogenic protein (BMP) measures such as BMP 2, 4, 6, and 7 don't show any significant changes between the groups. But at the same time, the VRT group shows positive improvement in inflammatory biomarkers (CRP, TNF-alpha, IL-2, IL-4, IL-6) analysis than the other two groups (P < 0.001). Our study suggests that including virtual reality training in PTOA shows beneficial changes in pain, functional disability, and modification of inflammatory biomarkers than sensory-motor training, but at the same time it shows a negligible effect on bone morphogenic proteins.

C-reactive protein (CRP) binds to several species of bacterial pathogens includingStreptococcus pneumoniae. Experiments in mice have revealed that one of the functions of CRP is to protect against pneumococcal infection by binding to pneumococci and activating the complement system. For protection, however, CRP must be injected into mice within a few hours of administering pneumococci, that is, CRP is protective against early-stage infection but not against late-stage infection. It is assumed that CRP cannot protect if pneumococci got time to recruit complement inhibitor factor H on their surface to become complement attack-resistant. Since the conformation of CRP is altered under inflammatory conditions and altered CRP binds to immobilized factor H also, we hypothesized that in order to protect against late-stage infection, CRP needed to change its structure and that was not happening in mice. Accordingly, we engineered CRP molecules (E-CRP) which bind to factor H on pneumococci but do not bind to factor H on any host cell in the blood. We found that E-CRP, in cooperation with wild-type CRP, was protective regardless of the timing of administering E-CRP into mice. We conclude that CRP acts via two different conformations to execute its anti-pneumococcal function and a model for the mechanism of action of CRP is proposed. These results suggest that pre-modified CRP, such as E-CRP, is therapeutically beneficial to decrease bacteremia in pneumococcal infection. Our findings may also have implications for infections with antibiotic-resistant pneumococcal strains and for infections with other bacterial species that use host proteins to evade complement-mediated killing.