Urinary Tract Infections Impair Adult Hippocampal Neurogenesis

Batoul Darwish; Farah Chamaa; Bassel Awada; Nada Lawand; Nayef E Saadé; Antoine G Abou Fayad; Wassim Abou-Kheir

doi:10.3390/biology11060891

Urinary Tract Infections Impair Adult Hippocampal Neurogenesis

Batoul Darwish, Farah Chamaa, Bassel Awada, Nada Lawand, Nayef E Saadé, Antoine G Abou Fayad, Wassim Abou-Kheir

Biological, Environmental Sciences and Engineering

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

Previous studies have suggested a link between urinary tract infections (UTIs) and cognitive impairment. One possible contributing factor for UTI-induced cognitive changes that has not yet been investigated is a potential alteration in hippocampal neurogenesis. In this study, we aim to investigate the effect of UTI on brain plasticity by specifically examining alterations in neurogenesis. Adult male Sprague Dawley rats received an intra-urethral injection of an Escherichia coli (E. coli) clinical isolate (108 CFU/mL). We found that rats with a UTI (CFU/mL ≥ 105) had reduced proliferation of neural stem cells (NSCs) at an early time point post infection (day 4) and neurogenesis at a later time point (day 34). This was associated with the decreased expression in mRNA of BDNF, NGF, and FGF2, and elevated expression of IL-1β in the hippocampus at 6 h post infection, but with no changes in optical intensity of the microglia and astrocytes. In addition, infected rats spent less time exploring a novel arm in the Y-maze test. Treatment with an anti-inflammatory drug did not revert the effect on NSCs, while treatment with antibiotics further decreased the basal level of their proliferation. This study presents novel findings on the impact of urinary tract infections on hippocampal neurogenesis that could be correlated with cognitive impairment.

Original language	English (US)
Pages (from-to)	891
Journal	Biology
Volume	11
Issue number	6
DOIs	https://doi.org/10.3390/biology11060891
State	Published - Jun 9 2022

Bibliographical note

KAUST Repository Item: Exported on 2022-06-27
Acknowledgements: The authors would like to acknowledge the National Council for Scientific Research of Lebanon (CNRS-L) for granting a doctoral fellowship to Batoul Darwish. The fellowship was offered in collaboration with the American University of Beirut. All authors have consented to this acknowledgement. This work was partly supported by the Medical Practice Plan (MPP) (grant: MPP-WAK-18).

ASJC Scopus subject areas

General Agricultural and Biological Sciences
General Biochemistry, Genetics and Molecular Biology
General Immunology and Microbiology

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10.3390/biology11060891

https://repository.kaust.edu.sa/bitstream/10754/679332/1/biology-11-00891-v2.pdf

Cite this

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title = "Urinary Tract Infections Impair Adult Hippocampal Neurogenesis",

abstract = "Previous studies have suggested a link between urinary tract infections (UTIs) and cognitive impairment. One possible contributing factor for UTI-induced cognitive changes that has not yet been investigated is a potential alteration in hippocampal neurogenesis. In this study, we aim to investigate the effect of UTI on brain plasticity by specifically examining alterations in neurogenesis. Adult male Sprague Dawley rats received an intra-urethral injection of an Escherichia coli (E. coli) clinical isolate (108 CFU/mL). We found that rats with a UTI (CFU/mL ≥ 105) had reduced proliferation of neural stem cells (NSCs) at an early time point post infection (day 4) and neurogenesis at a later time point (day 34). This was associated with the decreased expression in mRNA of BDNF, NGF, and FGF2, and elevated expression of IL-1β in the hippocampus at 6 h post infection, but with no changes in optical intensity of the microglia and astrocytes. In addition, infected rats spent less time exploring a novel arm in the Y-maze test. Treatment with an anti-inflammatory drug did not revert the effect on NSCs, while treatment with antibiotics further decreased the basal level of their proliferation. This study presents novel findings on the impact of urinary tract infections on hippocampal neurogenesis that could be correlated with cognitive impairment.",

author = "Batoul Darwish and Farah Chamaa and Bassel Awada and Nada Lawand and Saad{\'e}, {Nayef E} and {Abou Fayad}, {Antoine G} and Wassim Abou-Kheir",

note = "KAUST Repository Item: Exported on 2022-06-27 Acknowledgements: The authors would like to acknowledge the National Council for Scientific Research of Lebanon (CNRS-L) for granting a doctoral fellowship to Batoul Darwish. The fellowship was offered in collaboration with the American University of Beirut. All authors have consented to this acknowledgement. This work was partly supported by the Medical Practice Plan (MPP) (grant: MPP-WAK-18).",

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AU - Saadé, Nayef E

AU - Abou Fayad, Antoine G

AU - Abou-Kheir, Wassim

N1 - KAUST Repository Item: Exported on 2022-06-27 Acknowledgements: The authors would like to acknowledge the National Council for Scientific Research of Lebanon (CNRS-L) for granting a doctoral fellowship to Batoul Darwish. The fellowship was offered in collaboration with the American University of Beirut. All authors have consented to this acknowledgement. This work was partly supported by the Medical Practice Plan (MPP) (grant: MPP-WAK-18).

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N2 - Previous studies have suggested a link between urinary tract infections (UTIs) and cognitive impairment. One possible contributing factor for UTI-induced cognitive changes that has not yet been investigated is a potential alteration in hippocampal neurogenesis. In this study, we aim to investigate the effect of UTI on brain plasticity by specifically examining alterations in neurogenesis. Adult male Sprague Dawley rats received an intra-urethral injection of an Escherichia coli (E. coli) clinical isolate (108 CFU/mL). We found that rats with a UTI (CFU/mL ≥ 105) had reduced proliferation of neural stem cells (NSCs) at an early time point post infection (day 4) and neurogenesis at a later time point (day 34). This was associated with the decreased expression in mRNA of BDNF, NGF, and FGF2, and elevated expression of IL-1β in the hippocampus at 6 h post infection, but with no changes in optical intensity of the microglia and astrocytes. In addition, infected rats spent less time exploring a novel arm in the Y-maze test. Treatment with an anti-inflammatory drug did not revert the effect on NSCs, while treatment with antibiotics further decreased the basal level of their proliferation. This study presents novel findings on the impact of urinary tract infections on hippocampal neurogenesis that could be correlated with cognitive impairment.

AB - Previous studies have suggested a link between urinary tract infections (UTIs) and cognitive impairment. One possible contributing factor for UTI-induced cognitive changes that has not yet been investigated is a potential alteration in hippocampal neurogenesis. In this study, we aim to investigate the effect of UTI on brain plasticity by specifically examining alterations in neurogenesis. Adult male Sprague Dawley rats received an intra-urethral injection of an Escherichia coli (E. coli) clinical isolate (108 CFU/mL). We found that rats with a UTI (CFU/mL ≥ 105) had reduced proliferation of neural stem cells (NSCs) at an early time point post infection (day 4) and neurogenesis at a later time point (day 34). This was associated with the decreased expression in mRNA of BDNF, NGF, and FGF2, and elevated expression of IL-1β in the hippocampus at 6 h post infection, but with no changes in optical intensity of the microglia and astrocytes. In addition, infected rats spent less time exploring a novel arm in the Y-maze test. Treatment with an anti-inflammatory drug did not revert the effect on NSCs, while treatment with antibiotics further decreased the basal level of their proliferation. This study presents novel findings on the impact of urinary tract infections on hippocampal neurogenesis that could be correlated with cognitive impairment.

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JO - Biology

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ER -

Urinary Tract Infections Impair Adult Hippocampal Neurogenesis

Abstract

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