ABSTRACT
Many bacteria exploit host proteins for their colonization. Vitronectin (Vn), present in the blood and extracellular matrix, is one such protein that acts as a bridge between the bacteria and the host tissues leading to infection. In this study, Vn binding protein of Staphylococcus aureus (COL strain) (SaVnBP) has been characterized as autolysin(s) based on mass spectrometry data and the ability of these proteins to degrade S. aureus substratum. Deletion of the heparin-binding domain (residues 341-380) from the Vn did not affect its ability to interact with SaVnBP. Similarly, change of R to A or D to A in the second arginine-glycine-aspartic (RGD2) motif of Vn had no negative effect on protein-protein interaction. These results imply that the primary heparin-binding site and the second RGD motif of caprine Vn may not be involved in the initial step of S. aureus colonization.
Subject(s)
Carrier Proteins/metabolism , Heparin/metabolism , N-Acetylmuramoyl-L-alanine Amidase/metabolism , Oligopeptides/metabolism , Staphylococcus aureus/metabolism , Vitronectin/metabolism , Animals , Arginine/metabolism , Aspartic Acid/metabolism , Bacterial Proteins/metabolism , Extracellular Matrix , Glycine/metabolism , Goats/metabolism , Humans , Protein Binding/physiology , Somatomedins/metabolismABSTRACT
BACKGROUND: The ILEP Nerve Function Impairment in Reaction (INFIR) is a cohort study designed to identify predictors of reactions and nerve function impairment (NFI) in leprosy. AIM OF THE STUDY: Antibodies to mycobacteria, nerve components and serum cytokine were measured as potential markers for their possible association with reactions and NFI. PATIENTS AND METHODS: 303 newly diagnosed leprosy patients from two centres in North India were enrolled. Antibodies to PGL-1, LAM (IgG1 and IgG3), ceramide, S100 and TNFα levels were measured using ELISA techniques. RESULTS: S-100, PGL IgG and IgM antibody levels were lowest in patients with BT leprosy and highest in patients with lepromatous leprosy. LAM IgG1 and LAM IgG3 antibody levels were highest in patients with BL leprosy. Ceramide antibody levels were not correlated with type of leprosy. Levels of all the antibodies tested and TNF α were lowest in patients with only skin reaction. PGL IgM antibody levels were elevated in patients with skin reactions and NFI. Old sensory NFI is associated with significant elevation of PGL IgG, LAM IgG and S100 antibody levels. CONCLUSION: These results reveal that the antibody response to mycobacterial antigens, nerve antigens and cytokines are in a dynamic flux and could collectively contribute to NFI in leprosy. The association of multiple markers with old NFI may indicate the contribution of different pathological processes.
