Salmonella enterica serovar Typhi exposure elicits ex vivo cell-type-specific epigenetic changes in human gut cells

Sztein, Marcelo B.; Bafford, Andrea C; Salerno-Gonçalves, Rosângela

doi:10.1038/s41598-020-70492-2

Cited by 10 publications

(12 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several outstanding questions remain regarding the mechanism (s) of transcriptional and post-transcriptional regulation of HLA-G expression on MAIT cells. After S. Typhi exposure, MAIT cells undergo multiple coordinated modifications on Arg-me2(asy) and H4K20me3, H3K4me3, H4K20me1 epigenetic marks (47). Thus, epigenetic changes might be important in underlying these responses.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

B Cells Control Mucosal-Associated Invariant T Cell Responses to Salmonella enterica Serovar Typhi Infection Through the CD85j HLA-G Receptor

et al. 2021

Self Cite

View full text Add to dashboard Cite

Mucosal-associated invariant T (MAIT) cells are an innate-like population of T cells that display a TCR Vα7.2+ CD161+ phenotype and are restricted by the nonclassical MHC-related molecule 1 (MR1). Although B cells control MAIT cell development and function, little is known about the mechanisms underlying their interaction(s). Here, we report, for the first time, that during Salmonella enterica serovar Typhi (S. Typhi) infection, HLA-G expression on B cells downregulates IFN-γ production by MAIT cells. In contrast, blocking HLA-G expression on S. Typhi-infected B cells increases IFN-γ production by MAIT cells. After interacting with MAIT cells, kinetic studies show that B cells upregulate HLA-G expression and downregulate the inhibitory HLA-G receptor CD85j on MAIT cells resulting in their loss. These results provide a new role for HLA-G as a negative feedback loop by which B cells control MAIT cell responses to antigens.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Mass cytometry assays were performed as previously described with small modifications (47). Briefly, CD45-stained-B-LCL cells were co-cultured with PBMC containing MAIT cells in the presence of mAbs to CD107a and CD107b (15 ml of each/1 x 10 6 cells in 500 ml of R10 medium).…”

Section: Mass Cytometrymentioning

confidence: 99%

B Cells Control Mucosal-Associated Invariant T Cell Responses to Salmonella enterica Serovar Typhi Infection Through the CD85j HLA-G Receptor

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

“…To visualise the variance of 15 possible FCOM T-cell phenotypes, we performed principal component analysis (PCA) as described previously with small modifications. 56 Briefly, the calculation of principal components was performed by ClustVis web tools. 57 Columns were grouped using correlation distance (Pearson correlation subtracted from 1) and average linkages calculated.…”

Section: Discussionmentioning

confidence: 99%

Vaccine‐related major cutaneous reaction size correlates with cellular‐mediated immune responses after tularaemia immunisation

et al. 2021

View full text Add to dashboard Cite

Objectives. Francisella tularensis, the causative agent of tularaemia, is an exceptionally infectious bacterium, potentially fatal for humans if left untreated and with the potential to be developed as a bioweapon. Both natural infection and live-attenuated vaccine strain (LVS) confer good protection against tularaemia. LVS vaccination is traditionally administered by scarification, and the formation of a cutaneous reaction or take at the vaccination site is recognised as a clinical correlate of protection. Although previous studies have suggested that high antibody titres following vaccination might serve as a useful surrogate marker, the immunological correlates of protection remain unknown. Methods. We investigated the host Tcell-mediated immune (T-CMI) responses elicited following immunisation with LVS vaccine formulated by the DynPort Vaccine Company (DVC-LVS) or the United States Army Medical Research Institute of Infectious Diseases (USAMRIID-LVS). We compared T-CMI responses prompted by these vaccines and correlated them with take size. Results. We found that both LVS vaccines elicited similar T-CMI responses. Interestingly, take size associated with the T cells' ability to proliferate, secrete IFN-c and mobilise degranulation, suggesting that these responses play an essential role in tularaemia protection. Conclusions. These results renew the appreciation for vaccination through the scarification as a prime route of inoculation to target pathogens driving specific T-CMI responses and provide further evidence that T-CMI plays a role in protection from tularaemia.

show abstract

“…A recent study reported the impact of Salmonella infection on the early chromatin modifications occurring in the human gut microenvironment, which influence downstream immune responses in epithelial cells and immune cells [85] . S .…”

Section: Microbial Post-translational Modifications and Carcinogenesismentioning

confidence: 99%

“…[84] A recent study reported the impact of Salmonella infection on the early chromatin modifications occurring in the human gut microenvironment, which influence downstream immune responses in epithelial cells and immune cells. [85] S. Typhi-induced PTMs in histone methylation and acetylation associated with epithelial cells, natural killer T, mucosal-associated invariant T, T cell receptor-gd, monocytes, and CD8+ T-cells that are related to both gene activation and silencing. It found that arginine methylation might regulate the early differentiation of effector-memory CD4+ T-cells following exposure to S. Typhi.…”

Section: Microbial Post-translational Modifications and Carcinogenesismentioning

confidence: 99%

Impact of bacterial infection and intestinal microbiome on colorectal cancer development

Sun

2022

Chinese Medical Journal

View full text Add to dashboard Cite

Accumulating evidence suggests that intestinal bacteria play an important role in the pathogenesis of colorectal cancer (CRC). Due to the complexity of the intestinal microbiome, identification of the specific causative microbial agents in CRC remains challenging, and the search for the causative microbial agents is intense. However, whether bacteria or their products can induce inflammation that results in tumorigenesis or directly causes CRC in humans is still not clear. This review will mainly focus on the progress of bacterial infection and CRC, and introduce the microbial contribution to the hallmarks of cancer. This article uses Salmonella and its chronic infection as an example to investigate a single pathogen and its role in the development of CRC, based on laboratory and epidemiological evidence. The bacterial infection leads to an altered intestinal microbiome. The review also discusses the dysfunction of the microbiome and the mechanism of host–microbial interactions, for example, bacterial virulence factors, key signaling pathways in the host, and microbial post-translational modifications in the tumorigenesis. Colonic carcinogenesis involves a progressive accumulation of mutations in a genetically susceptible host leading to cellular autonomy. Moving forward, more human data are needed to confirm the direct roles of bacterial infection in CRC development. Insights into the inhibiting infection will help to prevent cancer and develop strategies to restore the balance between host and microorganisms.

show abstract

Salmonella enterica serovar Typhi exposure elicits ex vivo cell-type-specific epigenetic changes in human gut cells

Cited by 10 publications

References 53 publications

B Cells Control Mucosal-Associated Invariant T Cell Responses to Salmonella enterica Serovar Typhi Infection Through the CD85j HLA-G Receptor

B Cells Control Mucosal-Associated Invariant T Cell Responses to Salmonella enterica Serovar Typhi Infection Through the CD85j HLA-G Receptor

Vaccine‐related major cutaneous reaction size correlates with cellular‐mediated immune responses after tularaemia immunisation

Impact of bacterial infection and intestinal microbiome on colorectal cancer development

Contact Info

Product

Resources

About