Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models. / Skerniskyte, Jurate; Mulet, Céline; André, Antonin C.; Anderson, Mark C.; Injarabian, Louise; Buck, Achim; Prade, Verena M.; Sansonetti, Philippe J.; Reibel-Foisset, Sophie; Walch, Axel K.; Lebel, Michel; Lykkesfeldt, Jens; Marteyn, Benoit S.

In: Gut Microbes, Vol. 15, No. 2, 2271597, 2023.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Skerniskyte, J, Mulet, C, André, AC, Anderson, MC, Injarabian, L, Buck, A, Prade, VM, Sansonetti, PJ, Reibel-Foisset, S, Walch, AK, Lebel, M, Lykkesfeldt, J & Marteyn, BS 2023, 'Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models', Gut Microbes, vol. 15, no. 2, 2271597. https://doi.org/10.1080/19490976.2023.2271597

APA

Skerniskyte, J., Mulet, C., André, A. C., Anderson, M. C., Injarabian, L., Buck, A., Prade, V. M., Sansonetti, P. J., Reibel-Foisset, S., Walch, A. K., Lebel, M., Lykkesfeldt, J., & Marteyn, B. S. (2023). Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models. Gut Microbes, 15(2), [2271597]. https://doi.org/10.1080/19490976.2023.2271597

Vancouver

Skerniskyte J, Mulet C, André AC, Anderson MC, Injarabian L, Buck A et al. Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models. Gut Microbes. 2023;15(2). 2271597. https://doi.org/10.1080/19490976.2023.2271597

Author

Skerniskyte, Jurate ; Mulet, Céline ; André, Antonin C. ; Anderson, Mark C. ; Injarabian, Louise ; Buck, Achim ; Prade, Verena M. ; Sansonetti, Philippe J. ; Reibel-Foisset, Sophie ; Walch, Axel K. ; Lebel, Michel ; Lykkesfeldt, Jens ; Marteyn, Benoit S. / Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models. In: Gut Microbes. 2023 ; Vol. 15, No. 2.

Bibtex

@article{6ec2becfe8714e308d8334a4fc6caafc,
title = "Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models",
abstract = "Shigella spp. are the causative agents of bacterial dysentery and shigellosis, mainly in children living in developing countries. The study of Shigella entire life cycle in vivo and the evaluation of vaccine candidates{\textquoteright} protective efficacy have been hampered by the lack of a suitable animal model of infection. None of the studies evaluated so far (rabbit, guinea pig, mouse) allowed the recapitulation of full shigellosis symptoms upon Shigella oral challenge. Historical reports have suggested that dysentery and scurvy are both metabolic diseases associated with ascorbate deficiency. Mammals, which are susceptible to Shigella infection (humans, non-human primates and guinea pigs) are among the few species unable to synthesize ascorbate. We optimized a low-ascorbate diet to induce moderate ascorbate deficiency, but not scurvy, in guinea pigs to investigate whether poor vitamin C status increases the progression of shigellosis. Moderate ascorbate deficiency increased shigellosis symptom severity during an extended period of time (up to 48 h) in all strains tested (Shigella sonnei, Shigella flexneri 5a, and 2a). At late time points, an important influx of neutrophils was observed both within the disrupted colonic mucosa and in the luminal compartment, although Shigella was able to disseminate deep into the organ to reach the sub-mucosal layer and the bloodstream. Moreover, we found that ascorbate deficiency also increased Shigella penetration into the colon epithelium layer in a Gulo−/− mouse infection model. The use of these new rodent models of shigellosis opens new doors for the study of both Shigella infection strategies and immune responses to Shigella infection.",
keywords = "Animal models of GI infection or GI-diseases with microbial components, ascorbate deficiency, infection animal model, intestinal infection, Shigella, shigellosis",
author = "Jurate Skerniskyte and C{\'e}line Mulet and Andr{\'e}, {Antonin C.} and Anderson, {Mark C.} and Louise Injarabian and Achim Buck and Prade, {Verena M.} and Sansonetti, {Philippe J.} and Sophie Reibel-Foisset and Walch, {Axel K.} and Michel Lebel and Jens Lykkesfeldt and Marteyn, {Benoit S.}",
note = "Publisher Copyright: {\textcopyright} 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.",
year = "2023",
doi = "10.1080/19490976.2023.2271597",
language = "English",
volume = "15",
journal = "Gut Microbes",
issn = "1949-0976",
publisher = "Taylor & Francis",
number = "2",

}

RIS

TY - JOUR

T1 - Ascorbate deficiency increases progression of shigellosis in guinea pigs and mice infection models

AU - Skerniskyte, Jurate

AU - Mulet, Céline

AU - André, Antonin C.

AU - Anderson, Mark C.

AU - Injarabian, Louise

AU - Buck, Achim

AU - Prade, Verena M.

AU - Sansonetti, Philippe J.

AU - Reibel-Foisset, Sophie

AU - Walch, Axel K.

AU - Lebel, Michel

AU - Lykkesfeldt, Jens

AU - Marteyn, Benoit S.

N1 - Publisher Copyright: © 2023 The Author(s). Published with license by Taylor & Francis Group, LLC.

PY - 2023

Y1 - 2023

N2 - Shigella spp. are the causative agents of bacterial dysentery and shigellosis, mainly in children living in developing countries. The study of Shigella entire life cycle in vivo and the evaluation of vaccine candidates’ protective efficacy have been hampered by the lack of a suitable animal model of infection. None of the studies evaluated so far (rabbit, guinea pig, mouse) allowed the recapitulation of full shigellosis symptoms upon Shigella oral challenge. Historical reports have suggested that dysentery and scurvy are both metabolic diseases associated with ascorbate deficiency. Mammals, which are susceptible to Shigella infection (humans, non-human primates and guinea pigs) are among the few species unable to synthesize ascorbate. We optimized a low-ascorbate diet to induce moderate ascorbate deficiency, but not scurvy, in guinea pigs to investigate whether poor vitamin C status increases the progression of shigellosis. Moderate ascorbate deficiency increased shigellosis symptom severity during an extended period of time (up to 48 h) in all strains tested (Shigella sonnei, Shigella flexneri 5a, and 2a). At late time points, an important influx of neutrophils was observed both within the disrupted colonic mucosa and in the luminal compartment, although Shigella was able to disseminate deep into the organ to reach the sub-mucosal layer and the bloodstream. Moreover, we found that ascorbate deficiency also increased Shigella penetration into the colon epithelium layer in a Gulo−/− mouse infection model. The use of these new rodent models of shigellosis opens new doors for the study of both Shigella infection strategies and immune responses to Shigella infection.

AB - Shigella spp. are the causative agents of bacterial dysentery and shigellosis, mainly in children living in developing countries. The study of Shigella entire life cycle in vivo and the evaluation of vaccine candidates’ protective efficacy have been hampered by the lack of a suitable animal model of infection. None of the studies evaluated so far (rabbit, guinea pig, mouse) allowed the recapitulation of full shigellosis symptoms upon Shigella oral challenge. Historical reports have suggested that dysentery and scurvy are both metabolic diseases associated with ascorbate deficiency. Mammals, which are susceptible to Shigella infection (humans, non-human primates and guinea pigs) are among the few species unable to synthesize ascorbate. We optimized a low-ascorbate diet to induce moderate ascorbate deficiency, but not scurvy, in guinea pigs to investigate whether poor vitamin C status increases the progression of shigellosis. Moderate ascorbate deficiency increased shigellosis symptom severity during an extended period of time (up to 48 h) in all strains tested (Shigella sonnei, Shigella flexneri 5a, and 2a). At late time points, an important influx of neutrophils was observed both within the disrupted colonic mucosa and in the luminal compartment, although Shigella was able to disseminate deep into the organ to reach the sub-mucosal layer and the bloodstream. Moreover, we found that ascorbate deficiency also increased Shigella penetration into the colon epithelium layer in a Gulo−/− mouse infection model. The use of these new rodent models of shigellosis opens new doors for the study of both Shigella infection strategies and immune responses to Shigella infection.

KW - Animal models of GI infection or GI-diseases with microbial components

KW - ascorbate deficiency

KW - infection animal model

KW - intestinal infection

KW - Shigella

KW - shigellosis

U2 - 10.1080/19490976.2023.2271597

DO - 10.1080/19490976.2023.2271597

M3 - Journal article

C2 - 37876025

AN - SCOPUS:85174912738

VL - 15

JO - Gut Microbes

JF - Gut Microbes

SN - 1949-0976

IS - 2

M1 - 2271597

ER -

ID: 389409438