title: Exacerbation of group B streptococcal sepsis and arthritis in diabetic mice.
abstract: Group B streptococci (GBS) have been recognised as an ever-growing cause of serious invasive infections in non-pregnant adults, in particular in association with severe underlying diseases such as diabetes mellitus. In the present study we used mice rendered diabetic to gain further insights into host-pathogen interaction during induced GBS sepsis and septic arthritis. Type I diabetes was induced in adult CD-1 mice by low-dose streptozotocin treatment. Mice were then infected with different doses of GBS, and mortality, appearance of arthritis, growth of microorganisms in the organs and cytokine and chemokine profile were assessed in diabetic and control animals. The LD50 was significantly lower in diabetics than in controls, while both incidence and severity of arthritis were higher. A significantly higher number of microorganisms were recovered from the organs of diabetic mice than in controls. The worsening of sepsis and arthritis was associated with a significant increase in systemic and local production of IL-6, IL-1 beta, TNF-alpha, IL-10, macrophage inflammatory protein 1 alpha (MIP-1alpha), and MIP-2 and with a decrease in IFN-gamma production. Taken together, our results indicate an impaired host resistance to GBS infection in diabetics, likely due to a dysregulation of the cytokine network and prolonged local inflammatory response.
authors.affiliation: Sezione di Microbiologia, Dipartimento di Medicina Sperimentale e Scienze Biochimiche, Università degli Studi di Perugia, Via del Giochetto, 06122, Perugia Italy.
authors.forename: Manuela
authors.initials: M
authors.lastname: Puliti
authors.forename: Francesco
authors.initials: F
authors.lastname: Bistoni
authors.forename: Graziella
authors.initials: G
authors.lastname: Orefici
authors.forename: Luciana
authors.initials: L
authors.lastname: Tissi
mesh_terms: D000818:Animals; D001168:Arthritis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D016470:Bacteremia / Q000097:blood* / Q000276:immunology / Q000382:microbiology; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054426:Chemokine CXCL2; D018925:Chemokines / Q000276:immunology; D003921:Diabetes Mellitus, Experimental / Q000276:immunology / Q000382:microbiology*; D007371:Interferon-gamma / Q000276:immunology; D016753:Interleukin-10 / Q000276:immunology; D053583:Interleukin-1beta / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000276:immunology; D008297:Male; D051379:Mice; D013290:Streptococcal Infections / Q000150:complications* / Q000276:immunology / Q000382:microbiology; D013292:Streptococcus agalactiae / Q000302:isolation & purification*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D054405:Chemokine CCL3; D054407:Chemokine CCL4; D054426:Chemokine CXCL2; D018925:Chemokines; C404915:Cxcl2 protein, mouse; D053583:Interleukin-1beta; D015850:Interleukin-6; D019402:Macrophage Inflammatory Proteins; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma