title: Spontaneous arthritis in MRL/lpr mice is aggravated by Staphylococcus aureus and ameliorated by Nippostrongylus brasiliensis infections.
abstract: Rheumatoid arthritis is an autoimmune disease that affects human beings worldwide. Infections have been associated to autoimmune diseases because their ability to induce a dominant cytokine response. Joint inflammation has been related to Th1 response because they induce high expression of proinflammatory cytokines TNF-alpha, IL-1, IFN-gamma. MRL/lpr mice spontaneously develop an autoimmune disease affecting joints, kidneys, etc. We compared incidence and severity of arthritis, antibody response, cytokine production, in mice infected with bacteria or helminthes in the Murphy Roths Large (MRL)lpr mice. Infections with helminthes Heligmosomoides polygyrus, Nippostrongylus brasiliensis or bacteria Nocardia brasiliensis and Staphylococcus aureus were studied. IL-4, IFN-gamma and IgG1, IgG2a antibody productions were determined. IFN-gamma was increased in all groups, the highest production was observed after bacterial infection; IL-4 production was higher after helminthes infection. IgG1 sera levels were increased in the helminthes infected group. IgG2a sera concentration was stimulated by bacterial infection. The histopathology showed that 100% of bacterial infected mice developed arthritis and severe tissue damage such as cartilage erosion and bone destruction. Animals infected with parasites showed a decreased incidence and severity of arthritis. Severity of tissue damage in joints is correlated with increased numbers of lymphocytes and macrophages immunoreactive to proinflammatory cytokines.
authors.affiliation: Department of Immunology, Faculty of Medicine and University Hospital, Monterrey, Mexico. msalinas@hu.uanl.mx
authors.forename: Mario C
authors.initials: MC
authors.lastname: Salinas-Carmona
authors.forename: Guadalupe
authors.initials: G
authors.lastname: de la Cruz-Galicia
authors.forename: Isabel
authors.initials: I
authors.lastname: Pérez-Rivera
authors.forename: Juan M
authors.initials: JM
authors.lastname: Solís-Soto
authors.forename: Juan C
authors.initials: JC
authors.lastname: Segoviano-Ramirez
authors.forename: Anna Velia
authors.initials: AV
authors.lastname: Vázquez
authors.forename: Mario A
authors.initials: MA
authors.lastname: Garza
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood; D000909:Antibodies, Helminth / Q000097:blood; D001169:Arthritis, Experimental / Q000276:immunology / Q000503:physiopathology*; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000503:physiopathology*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D051379:Mice; D019463:Mice, Inbred MRL lpr; D009559:Nippostrongylus / Q000276:immunology* / Q000472:pathogenicity; D012720:Severity of Illness Index; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D013211:Staphylococcus aureus / Q000276:immunology* / Q000378:metabolism / Q000472:pathogenicity; D017206:Strongylida Infections / Q000276:immunology / Q000503:physiopathology; D018417:Th1 Cells / Q000276:immunology
chemical_list: D000907:Antibodies, Bacterial; D000909:Antibodies, Helminth; D016207:Cytokines