alpha-Neup5Ac-(2--3)-beta-D-Galp-(1--4)-[alpha-L-Fucp-(1--3)]-D-GlcpNAc and Streptococcal-Infections

Streptococcus pyogenes tonsillar infection is well known to trigger and exacerbate psoriasis lesions in both guttate and plaque forms of the disease. Although mucosal and cutaneous tissues are closely involved in psoriasis pathology, the interaction between their specific immune responses has not been deeply explored. This work aims to address and characterize the presence of humoral responses against S. pyogenes in patients with psoriasis and its putative association with cytokine responses detected in vitro in our psoriasis ex vivo model, based on the coculture of cutaneous lymphocyte-associated antigen

Topics: Adult; Cytokines; Epidermal Cells; Female; Humans; Immunoglobulin A; Immunoglobulin G; Interleukin-17; Male; Middle Aged; Oligosaccharides; Palatine Tonsil; Psoriasis; Sialyl Lewis X Antigen; Skin; Streptococcal Infections; Streptococcus pyogenes; T-Lymphocytes; Young Adult

The expression of sialy-Lewis(x) (sLe(x); Neu5Ac alpha 2-3 Gal beta 1-4) (Fuc alpha 1-3) GlcNAc-R) on oral bacteria producing infective endocarditis was determined by a whole-cell enzyme linked immunosorbent assay and an immunoelectron microscopy using the well-characterized anti-sLe(x) monoclonal antibody SNH-3 (mAb SNH-3; IgM class). mAb SNH-3 reacted strongly with whole cells of oral bacteria: Streptococcus sanguis, Streptococcus mutans, Streptococcus mitis, Streptococcus salivarius, Streptococcus intermedius, Streptococcus constellatus, Streptococcus anginosus, Streptococcus pyogenes, Actinobacillus actinomycetemcomitans, Eikenella corrodens and Porphyromonas gingivalis. The negatively stained immuno-electron micrograph of Streptococcus pyogenes showed many reactive gold particles on the cell surface. Our findings demonstrated the existence of immunologic mimicry between the sLe(x) oligosaccharide and cell surface antigens of many species associated with infective endocarditis. We propose the hypothesis that if these bacteria escape their normal habitats, the surface components that mimic the sLe(x) oligosaccharide might bind to host antigens of the selectin family which could promote binding to endothelial cells and, consequently, initiation of the events leading to infective endocarditis.

Topics: Antibodies, Monoclonal; Antigens, Bacterial; Bacteria; Bacterial Adhesion; Carbohydrate Sequence; Cross Reactions; Endocarditis, Bacterial; Humans; Microscopy, Immunoelectron; Molecular Sequence Data; Mouth; Oligosaccharides; Selectins; Sialyl Lewis X Antigen; Streptococcal Infections; Streptococcus; Streptococcus pyogenes