Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection
Jéssica da Conceição Mendonça,
João Matheus Sobral Pena,
Noemi dos Santos Macêdo,
Dayane de Souza Rodrigues,
Dayane Alvarinho de Oliveira,
Brady L. Spencer,
Eduardo José Lopes-Torres,
Lindsey R. Burcham,
Kelly S. Doran,
Prescilla Emy Nagao
Affiliations
Jéssica da Conceição Mendonça
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
João Matheus Sobral Pena
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
Noemi dos Santos Macêdo
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
Dayane de Souza Rodrigues
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
Dayane Alvarinho de Oliveira
Laboratório de Helmintologia Romero Lascasas Porto, Department of Immunology, Microbiology e Parasitology, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
Brady L. Spencer
Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 12800, USA
Eduardo José Lopes-Torres
Laboratório de Helmintologia Romero Lascasas Porto, Department of Immunology, Microbiology e Parasitology, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
Lindsey R. Burcham
Department of Microbiology, University of Tennessee Knoxville, Knoxville, TN 37916, USA
Kelly S. Doran
Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 12800, USA
Prescilla Emy Nagao
Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, Brazil
Streptococcus agalactiae (Group B Streptococcus, GBS) is the leading cause of neonatal sepsis and meningitis but has been recently isolated from non-pregnant adults with underlying medical conditions like diabetes. Despite diabetes being a key risk factor for invasive disease, the pathological consequences during GBS infection remain poorly characterized. Here, we demonstrate the pathogenicity of the GBS90356-ST17 and COH1-ST17 strains in streptozotocin-induced diabetic mice. We show that GBS can spread through the bloodstream and colonize several tissues, presenting a higher bacterial count in diabetic-infected mice when compared to non-diabetic-infected mice. Histological sections of the lungs showed inflammatory cell infiltration, collapsed septa, and red blood cell extravasation in the diabetic-infected group. A significant increase in collagen deposition and elastic fibers were also observed in the lungs. Moreover, the diabetic group presented red blood cells that adhered to the valve wall and disorganized cardiac muscle fibers. An increased expression of KC protein, IL-1β, genes encoding immune cell markers, and ROS (reactive oxygen species) production was observed in diabetic-infected mice, suggesting GBS promotes high levels of inflammation when compared to non-diabetic animals. Our data indicate that efforts to reverse the epidemic of diabetes could considerably reduce the incidence of invasive infection, morbidity and mortality due to GBS.
