Despite the fact that closely related bacteria can cause different levels of disease, the genetic changes that cause some isolates to be more pathogenic than others are generally not well understood. We use a combination of approaches to determine which factors contribute to the increased virulence of a Bordetella bronchiseptica lineage. A strain isolated from a host with B. bronchiseptica-induced disease, strain 1289, was 60-fold more virulent in mice than one isolated from an asymptomatically infected host, strain RB50. Transcriptome analysis and quantitative reverse transcription-PCR showed that the type III secretion system (TTSS) genes were more highly expressed by strain 1289 than strain RB50. Compared to strain RB50, strain 1289 exhibited greater TTSS-mediated cytotoxicity of a mammalian cell line. Additionally, we show that the increase in virulence of strain 1289 compared to that of RB50 was partially attributable to the TTSS. Using multilocus sequence typing, we identified another strain from the same lineage as strain 1289. Similar to strain 1289, we implicate the TTSS in the increased virulence of this strain. Together, our data suggest that the TTSS is involved in the increased virulence of a B. bronchiseptica lineage which appears to be disproportionately associated with disease. These data are consistent with the view that B. bronchiseptica lineages can have different levels of virulence, which may contribute to this species' ability to cause different severities of respiratory disease.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738013 | PMC |
http://dx.doi.org/10.1128/IAI.01362-08 | DOI Listing |
Arch Virol
December 2024
School of Biotechnology, Jawaharlal Nehru University, 110067, New Delhi, India.
Targeting interactions between a virus and a host protein is one of the important approaches to developing antiviral therapies. We previously identified host nucleolin as a novel interacting partner of the influenza A virus nucleoprotein, and it was demonstrated that this interaction restricts virus replication. In the current study, we examined the interaction of nucleolin with the viral nucleoprotein at the domain and amino acid levels using in vitro and in silico approaches.
View Article and Find Full Text PDFGenes (Basel)
November 2024
School of Biological & Chemical Engineering, Zhejiang University of Science & Technology, Hangzhou 310023, China.
J Funct Morphol Kinesiol
November 2024
Department of Medicine and Surgery, University of Parma, Via Gramsci 14, 43126 Parma, Italy.
Background: The impact of prolonged digital device exposure on physical and mental health in children has been widely investigated by the scientific community. Additionally, the lockdown periods due to the COVID-19 pandemic further exposed children to screen time for e-learning activities. The aim of this systematic review (PROSPERO Registration: CRD42022315596) was to evaluate the effect of digital device exposure on children's health.
View Article and Find Full Text PDFGut Microbes
November 2024
Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Undernutrition in children commonly disrupts the structure and function of the small intestinal microbial community, leading to enteropathies, compromised metabolic health, and impaired growth and development. The mechanisms by which diet and microbes mediate the balance between commensal and pathogenic intestinal flora remain elusive. In a murine model of undernutrition, we investigated the direct interactions , a prevalent small intestinal pathogen, on indigenous microbiota and specifically on Lactobacillus strains known for their mucosal and growth homeostatic properties.
View Article and Find Full Text PDFPharmaceutics
September 2024
Institute for Clinical and Molecular Virology, Friedrich-Alexander University of Erlangen-Nürnberg (FAU), Schlossgarten 4, 91054 Erlangen, Germany.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!