Abstract
BackgroundS. aureus biofilm serves a major role in pathogenesis. Two of the major components of bacterial biofilm are Polysaccharides intercellular adhesions (PIA) and surface proteins. It is not known how PIA and surface proteins expressions are affected in presence of blood serum. Analyses of surface proteins expressions will provide more effective biomarker discovery that might lead to development of antimicrobial therapeutics to meet the challenges of biofilm-related infections.MethodSecondary cultures of S. aureus Philips, a biofilm-forming bacterium, were generated by inoculating 1 ml of overnight culture into 50 ml of TSB. Bacteria were cultured at several concentrations of blood serum and found that 12.5% supplemented blood serum provide s similar growth curve as normal TSB (100%). One and 2 D SASPAGE were used to separate proteins and the differentially expressed proteins were identified by nano-LC/MS.ResultsPolysaccharide intercellular adhesions production was significantly increased due to the addition of blood serum in the media. We also identified two serum proteins, apolipoprotein and globulin (Fc and Fab), that remained attached with the membrane fraction of bacterial proteins.ConclusionThese results have strongly demonstrated that blood serum influences the exopolysaccharide expression in S. aureus.
Highlights
Hepatitis C virus (HCV) infection accounts for almost 3% of the world’s population [1]
Biochemical responses in responder and non-responders: It is clearly stated that biochemical parameters like LFT, AST and ALT are correlated with therapy outcome.The values of these parameters are decreased in responders while increased in nonresponders representing that hepatitis C virus played a vital role to make changes in non-responders
Cytokines play a vital role in viral clearance, control of infection, swelling, restoration, fibrosis and are concerned in the irrational procedures arising in the liver throughout viral infection [9]
Summary
Hepatitis C virus (HCV) infection accounts for almost 3% of the world’s population [1]. The pathogenicity of viral infections are highly predisposed by the host immune response. Immune system of the body eradicate several viruses at their acute stage, though HBV (hepatitis B virus) and HCV (hepatitis C virus) can evade the host immune system and develop persistent infection [3]. IL-12 expresses antiviral role as an activator of natural killer cells, inducer of interferon γ, and cytotoxic lymphocytes. These all factors are vital part of anti-HCV immune responses [6]. This study was intended to explore the expression of IL-12 in interferon responders and non-responders of hepatitis C infection and to assess their possible role as new biomarker for the treatment response
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