Resistant Salmonella Typhi in Zambia
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REPOSITORIES: ENA
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Project description:Genomic Signature of Multi-Drug Resistant Salmonella Typhi related to a Massive Outbreak in Zambia during 2010 - 2012.
| PRJEB7179 | ENA
Project description:Genomic Signature of Multi-Drug Resistant Salmonella Typhi related to a Massive Outbreak in Zambia during 2010 - 2012 _part 02
| PRJEB7182 | ENA
Project description:Outbreak of Salmonella Typhi
| PRJEB54812 | ENA
Project description:Salmonella Typhi (S. Typhi), the causative agent of typhoid disease, remains a major public health concern. Owing to the human-restricted nature of S. Typhi, current studies of typhoid pathogenesis in animal models are limited to a murine non-typhoidal pathogen. Furthermore, human studies are limited to analyses of peripheral immune responses which are blind to tissue-specific immunity and do not allow perturbations. What is now needed is an integrative approach that will provide mechanistic insights into S. typhi pathogenesis and immune correlates of infection outcome. Here, we performed an integrated single-cell analysis of immune responses from the human S. Typhi challenge model and mouse model of typhoid disease, to associate biological mechanism with human infection outcome. Most prominent, we revealed immune subsets with a hypoxia-related signature in circulating immune cells from individuals that develop disease in the human challenge model. This signature was also evident in the mouse model in activated macrophages infiltrating into the Peyer’s patches, but not during infection with a mutant strain impaired for gut invasion. We further identified hypoxia-related signature as a general immune correlate of disease outcome in other infection- and inflammatory- related diseases. Collectively, using integrated analysis of mouse and human infection models, we revealed a hypoxia-related signature that link immune responses during bacterial invasion to increased risk of developing typhoid disease in humans, suggesting a possible causative role during the development of typhoid disease.
2025-07-02 | GSE285646 | GEO
Project description:Salmonella Typhi (S. Typhi), the causative agent of typhoid disease, remains a major public health concern. Owing to the human-restricted nature of S. Typhi, current studies of typhoid pathogenesis in animal models are limited to a murine non-typhoidal pathogen. Furthermore, human studies are limited to analyses of peripheral immune responses which are blind to tissue-specific immunity and do not allow perturbations. What is now needed is an integrative approach that will provide mechanistic insights into S. typhi pathogenesis and immune correlates of infection outcome. Here, we performed an integrated single-cell analysis of immune responses from the human S. Typhi challenge model and mouse model of typhoid disease, to associate biological mechanism with human infection outcome. Most prominent, we revealed immune subsets with a hypoxia-related signature in circulating immune cells from individuals that develop disease in the human challenge model. This signature was also evident in the mouse model in activated macrophages infiltrating into the Peyer’s patches, but not during infection with a mutant strain impaired for gut invasion. We further identified hypoxia-related signature as a general immune correlate of disease outcome in other infection- and inflammatory- related diseases. Collectively, using integrated analysis of mouse and human infection models, we revealed a hypoxia-related signature that link immune responses during bacterial invasion to increased risk of developing typhoid disease in humans, suggesting a possible causative role during the development of typhoid disease.
2025-07-02 | GSE285645 | GEO
Project description:Fluoroquinolone-resistant Cambodian Salmonella typhi
| PRJEB70293 | ENA
Project description:Ceftriaxone resistant H58 Salmonella Typhi
| PRJEB21155 | ENA
Project description:Salmonella Typhi (S. Typhi), the causative agent of typhoid disease, remains a major public health concern. Owing to the human-restricted nature of S. Typhi, current studies of typhoid pathogenesis in animal models are limited to a murine non-typhoidal pathogen. Furthermore, human studies are limited to analyses of peripheral immune responses which are blind to tissue-specific immunity and do not allow perturbations. What is now needed is an integrative approach that will provide mechanistic insights into S. typhi pathogenesis and immune correlates of infection outcome. Here, we performed an integrated single-cell analysis of immune responses from the human S. Typhi challenge model and mouse model of typhoid disease, to associate biological mechanism with human infection outcome. Most prominent, we revealed immune subsets with a hypoxia-related signature in circulating immune cells from individuals that develop disease in the human challenge model. This signature was also evident in the mouse model in activated macrophages infiltrating into the Peyer’s patches, but not during infection with a mutant strain impaired for gut invasion. We further identified hypoxia-related signature as a general immune correlate of disease outcome in other infection- and inflammatory- related diseases. Collectively, using integrated analysis of mouse and human infection models, we revealed a hypoxia-related signature that link immune responses during bacterial invasion to increased risk of developing typhoid disease in humans, suggesting a possible causative role during the development of typhoid disease.
2025-07-02 | GSE285641 | GEO
Project description:Human genetic diversity can reveal critical factors in host-pathogen interactions. This is especially useful for human-restricted pathogens like Salmonella enterica serovar Typhi (S. Typhi), the cause of Typhoid fever. One key dynamic during infection is competition for nutrients: host cells attempt to restrict intracellular replication by depriving bacteria of key nutrients or delivering toxic metabolites in a process called nutritional immunity. Here, a cellular genome-wide association study of intracellular replication by S. Typhi in nearly a thousand cell lines from around the world—and extensive follow-up using intracellular S. Typhi transcriptomics and manipulation of magnesium concentrations—demonstrates that the divalent cation channel mucolipin-2 (MCOLN2) restricts S. Typhi intracellular replication through magnesium deprivation. Our results reveal natural diversity in Mg2+ limitation as a key component of nutritional immunity against S. Typhi.
2023-01-05 | GSE222194 | GEO
Project description:Salmonella Typhi (S. Typhi), the causative agent of typhoid disease, remains a major public health concern. Owing to the human-restricted nature of S. Typhi, current studies of typhoid pathogenesis in animal models are limited to a murine non-typhoidal pathogen. Furthermore, human studies are limited to analyses of peripheral immune responses which are blind to tissue-specific immunity and do not allow perturbations. What is now needed is an integrative approach that will provide mechanistic insights into S. typhi pathogenesis and immune correlates of infection outcome. Here, we performed an integrated single-cell analysis of immune responses from the human S. Typhi challenge model and mouse model of typhoid disease, to associate biological mechanism with human infection outcome. Most prominent, we revealed immune subsets with a hypoxia-related signature in circulating immune cells from individuals that develop disease in the human challenge model. This signature was also evident in the mouse model in activated macrophages infiltrating into the Peyer’s patches, but not during infection with a mutant strain impaired for gut invasion. We further identified hypoxia-related signature as a general immune correlate of disease outcome in other infection- and inflammatory- related diseases. Collectively, using integrated analysis of mouse and human infection models, we revealed a hypoxia-related signature that link immune responses during bacterial invasion to increased risk of developing typhoid disease in humans, suggesting a possible causative role during the development of typhoid disease.
2025-07-02 | GSE285642 | GEO