Salmonella infection induces the reorganization of follicular dendritic cell networks concomitant with the failure to generate germinal centers

Marcial‐Juárez, Edith; Pérez-Toledo, Marisol; Nayar, Saba; Pipi, Elena; Alshayea, Areej; Persaud, Ruby; Jossi, Sian; Lamerton, Rachel E.; Barone, Francesca; Henderson, Ian; Cunningham, Adam F.

doi:10.1016/j.isci.2023.106310

Cited by 3 publications

(1 citation statement)

References 72 publications

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“…Flow cytometry was performed as described previously 8,39,40 . Splenocytes were resuspended in FACS buffer in a 96-well V-bottom plates at 2.5 x 10 6 cells with blocking reagent (anti-CD16/CD32) for 15 minutes at 4 °C.…”

Section: Flow Cytometrymentioning

confidence: 99%

Wild-type and single-O-antigen repeat outer-membrane vesicles induce equivalent protection against homologous and heterologousSalmonellachallenge

Alshayea,

Jossi,

Marcial-Juárez

et al. 2024

Preprint

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Lipopolysaccharide O-antigen is an immunodominant target of protective antibodies. Variation in O-antigen structures limits antibody-mediated cross-protection between closely-related pathogens includingSalmonellaTyphimurium (STm) andS. Enteritidis (SEn). Bacterial outer membrane vesicles (OMV) are vaccine platforms presenting surface antigens in their natural conformations. To assess how O-antigen lengths impact antibody responses and control of homologous or heterologous infection, mice were immunized with STm-OMV containing wild-type O-antigen unit repeats (wt-OMV), ≤1 O-antigen unit (wzy-OMV), or no O-antigen units (wbaP-OMV) respectively and challenged with either STm or SEn. Unexpectedly, anti-STm LPS IgG and protection to STm were comparable after immunization with either wt-OMV or wzy-OMV. Anti-porin responses were elevated after immunization with wzy-OMV and wbaP-OMV. A single immunization with any OMV induced minimal cross-protection against SEn, except in blood. In contrast, boosting with O-antigen-expressing OMV enhanced control of SEn infections by >10-fold. These results suggest that i) Antibody to single or variable-length O-antigen units are comparably protective againstSalmonella; ii) Antigens other than immunodominant O-antigens may be targets of cross-reactive antibodies that moderate bacterial burdens; iii) Boosting can enhance the level of cross-protection against relatedSalmonellaserovars and iv) High tissue burdens ofSalmonellacan be present in the absence of detectable bacteraemia.

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Section: Flow Cytometrymentioning

confidence: 99%

Wild-type and single-O-antigen repeat outer-membrane vesicles induce equivalent protection against homologous and heterologousSalmonellachallenge

Alshayea,

Jossi,

Marcial-Juárez

et al. 2024

Preprint

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The follicular dendritic cell: At the germinal center of autoimmunity?

Krimpenfort,

Degn,

Heesters

2024

Cell Reports

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Dysregulation of Stress Erythropoiesis and Enhanced Susceptibility to Salmonella Typhimurium Infection in Aryl Hydrocarbon Receptor–Deficient Mice

Mayer,

Cengiz-Dartenne,

Thiem

et al. 2024

The Journal of Infectious Diseases

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Background By acting as an environmental sensor, the ligand-induced transcription factor aryl hydrocarbon receptor (AhR) regulates acute innate and adaptive immune responses against pathogens. Here, we analyzed the function of AhR in a model for chronic systemic infection with attenuated Salmonella Typhimurium (STM). Methods WT and AhR-deficient mice were infected with the attenuated STM strain TAS2010 and analyzed for bacterial burden, host defense functions and inflammatory stress erythropoiesis. Results AhR-deficient mice were highly susceptible to TAS2010 infection compared with WT mice demonstrated by reduced bacterial clearance and increased mortality. STM infection resulted in macrocytic anemia and enhanced splenomegaly along with destruction of the splenic architecture in AhR-deficient mice. In addition, AhR-deficient mice displayed a major expansion of splenic immature red blood cells, indicative of infection-induced stress erythropoiesis. Elevated serum levels of erythropoietin and interleukin-6 upon infection as well as increased numbers of splenic stress erythroid progenitors already in steady state probably drive this effect and might cause the alterations in splenic immune cell compartments, thereby preventing an effective host defense against STM in AhR-deficient mice. Conclusions AhR-deficient mice fail to clear chronic TAS2010 infection due to enhanced stress erythropoiesis in the spleen and accompanying destruction of the splenic architecture.

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Salmonella infection induces the reorganization of follicular dendritic cell networks concomitant with the failure to generate germinal centers

Cited by 3 publications

References 72 publications

Wild-type and single-O-antigen repeat outer-membrane vesicles induce equivalent protection against homologous and heterologousSalmonellachallenge

Wild-type and single-O-antigen repeat outer-membrane vesicles induce equivalent protection against homologous and heterologousSalmonellachallenge

The follicular dendritic cell: At the germinal center of autoimmunity?

Dysregulation of Stress Erythropoiesis and Enhanced Susceptibility to Salmonella Typhimurium Infection in Aryl Hydrocarbon Receptor–Deficient Mice

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