Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection
<i>Streptococcus agalactiae</i> (Group B <i>Streptococcus</i>, 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 in...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-04-01
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| Series: | Pathogens |
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| Online Access: | https://www.mdpi.com/2076-0817/12/4/580 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Jéssica da Conceição Mendonça |
| collection | DOAJ |
| description | <i>Streptococcus agalactiae</i> (Group B <i>Streptococcus</i>, 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. |
| first_indexed | 2024-03-11T04:39:05Z |
| format | Article |
| id | doaj.art-2f9920e756244488becddb7fca0c825c |
| institution | Directory Open Access Journal |
| issn | 2076-0817 |
| language | English |
| last_indexed | 2024-03-11T04:39:05Z |
| publishDate | 2023-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Pathogens |
| spelling | doaj.art-2f9920e756244488becddb7fca0c825c2023-11-17T20:48:44ZengMDPI AGPathogens2076-08172023-04-0112458010.3390/pathogens12040580Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 InfectionJéssica da Conceição Mendonça0João Matheus Sobral Pena1Noemi dos Santos Macêdo2Dayane de Souza Rodrigues3Dayane Alvarinho de Oliveira4Brady L. Spencer5Eduardo José Lopes-Torres6Lindsey R. Burcham7Kelly S. Doran8Prescilla Emy Nagao9Laboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, BrazilLaboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, BrazilLaboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, BrazilLaboratory of Molecular Biology and Physiology of Streptococci, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, BrazilLaboratório de Helmintologia Romero Lascasas Porto, Department of Immunology, Microbiology e Parasitology, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, BrazilDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 12800, USALaboratório de Helmintologia Romero Lascasas Porto, Department of Immunology, Microbiology e Parasitology, Rio de Janeiro State University, Rio de Janeiro 20550-013, RJ, BrazilDepartment of Microbiology, University of Tennessee Knoxville, Knoxville, TN 37916, USADepartment of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, CO 12800, USALaboratory 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<i>Streptococcus agalactiae</i> (Group B <i>Streptococcus</i>, 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.https://www.mdpi.com/2076-0817/12/4/580<i>Streptococcus agalactiae</i>Group B <i>Streptococcus</i>diabetes <i>mellitus</i>bacterial dissemination |
| spellingShingle | 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 Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection Pathogens <i>Streptococcus agalactiae</i> Group B <i>Streptococcus</i> diabetes <i>mellitus</i> bacterial dissemination |
| title | Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection |
| title_full | Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection |
| title_fullStr | Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection |
| title_full_unstemmed | Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection |
| title_short | Enhanced Vulnerability of Diabetic Mice to Hypervirulent <i>Streptococcus agalactiae</i> ST-17 Infection |
| title_sort | enhanced vulnerability of diabetic mice to hypervirulent i streptococcus agalactiae i st 17 infection |
| topic | <i>Streptococcus agalactiae</i> Group B <i>Streptococcus</i> diabetes <i>mellitus</i> bacterial dissemination |
| url | https://www.mdpi.com/2076-0817/12/4/580 |
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