Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.
Identifieur interne : 000C39 ( PubMed/Checkpoint ); précédent : 000C38; suivant : 000C40Differential neurodegenerative phenotypes are associated with heterogeneous voiding dysfunction in a coronavirus-induced model of multiple sclerosis.
Auteurs : Sanghee Lee [États-Unis] ; Balachandar Nedumaran [États-Unis] ; Joseph Hypolite [États-Unis] ; Brian Caldwell [États-Unis] ; Michael C. Rudolph [États-Unis] ; Anna P. Malykhina [États-Unis]Source :
- Scientific reports [ 2045-2322 ] ; 2019.
Abstract
Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE). Long-term follow up study revealed three phenotypes of neurodegenerative symptom development: recovery (REC group), chronic progression (C-PRO group) and chronic disease with relapsing-remitting episodes (C-RELAP group). The levels of IL-1β in REC group, IL-10 in C-RELAP group, and IL-1β, IL-6, IL-10 and TNF-α in C-PRO group were diminished in the brain. The levels of TNF-α in REC group and INF-γ, IL-2, TGF-β and TNF-α in the C-PRO group were also diminished in the urinary bladder. Mice in C-RELAP group showed a delayed recovery of voiding function. In vitro contractility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated contractions in C-RELAP group, whereas C-PRO group had elevated muscle-mediated contractions. In conclusion, mice with CIE developed three phenotypes of neurologic impairment mimicking different types of MS progression in humans and showed differential mechanisms driving neurogenic bladder dysfunction.
DOI: 10.1038/s41598-019-47407-x
PubMed: 31350464
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<front><div type="abstract" xml:lang="en">Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE). Long-term follow up study revealed three phenotypes of neurodegenerative symptom development: recovery (REC group), chronic progression (C-PRO group) and chronic disease with relapsing-remitting episodes (C-RELAP group). The levels of IL-1β in REC group, IL-10 in C-RELAP group, and IL-1β, IL-6, IL-10 and TNF-α in C-PRO group were diminished in the brain. The levels of TNF-α in REC group and INF-γ, IL-2, TGF-β and TNF-α in the C-PRO group were also diminished in the urinary bladder. Mice in C-RELAP group showed a delayed recovery of voiding function. In vitro contractility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated contractions in C-RELAP group, whereas C-PRO group had elevated muscle-mediated contractions. In conclusion, mice with CIE developed three phenotypes of neurologic impairment mimicking different types of MS progression in humans and showed differential mechanisms driving neurogenic bladder dysfunction.</div>
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<Abstract><AbstractText>Patients with multiple sclerosis (MS) develop a variety of lower urinary tract symptoms (LUTS). We previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic strain of a coronavirus. In the present study, we further study the role of long-lasting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus induced encephalitis (CIE). Long-term follow up study revealed three phenotypes of neurodegenerative symptom development: recovery (REC group), chronic progression (C-PRO group) and chronic disease with relapsing-remitting episodes (C-RELAP group). The levels of IL-1β in REC group, IL-10 in C-RELAP group, and IL-1β, IL-6, IL-10 and TNF-α in C-PRO group were diminished in the brain. The levels of TNF-α in REC group and INF-γ, IL-2, TGF-β and TNF-α in the C-PRO group were also diminished in the urinary bladder. Mice in C-RELAP group showed a delayed recovery of voiding function. In vitro contractility studies determined a decreased basal detrusor tone and reduced amplitude of nerve-mediated contractions in C-RELAP group, whereas C-PRO group had elevated muscle-mediated contractions. In conclusion, mice with CIE developed three phenotypes of neurologic impairment mimicking different types of MS progression in humans and showed differential mechanisms driving neurogenic bladder dysfunction.</AbstractText>
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<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Californie</li>
</region>
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<tree><country name="États-Unis"><region name="Californie"><name sortKey="Lee, Sanghee" sort="Lee, Sanghee" uniqKey="Lee S" first="Sanghee" last="Lee">Sanghee Lee</name>
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<name sortKey="Caldwell, Brian" sort="Caldwell, Brian" uniqKey="Caldwell B" first="Brian" last="Caldwell">Brian Caldwell</name>
<name sortKey="Hypolite, Joseph" sort="Hypolite, Joseph" uniqKey="Hypolite J" first="Joseph" last="Hypolite">Joseph Hypolite</name>
<name sortKey="Malykhina, Anna P" sort="Malykhina, Anna P" uniqKey="Malykhina A" first="Anna P" last="Malykhina">Anna P. Malykhina</name>
<name sortKey="Nedumaran, Balachandar" sort="Nedumaran, Balachandar" uniqKey="Nedumaran B" first="Balachandar" last="Nedumaran">Balachandar Nedumaran</name>
<name sortKey="Rudolph, Michael C" sort="Rudolph, Michael C" uniqKey="Rudolph M" first="Michael C" last="Rudolph">Michael C. Rudolph</name>
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