Please use this identifier to cite or link to this item:
http://sgc.anlis.gob.ar/handle/123456789/2450
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Arenas-Mosquera, David | es |
dc.contributor.author | Pinto, Alipio | es |
dc.contributor.author | Cerny, Natacha | es |
dc.contributor.author | Berdasco, Clara | es |
dc.contributor.author | Cangelosi, Adriana | es |
dc.contributor.author | Geoghegan, Patricia A. | es |
dc.contributor.author | Malchiodi, Emilio Luis | es |
dc.contributor.author | De Marzi, Mauricio C | es |
dc.contributor.author | Goldstein, Jorge | es |
dc.date.accessioned | 2022-08-17T16:48:45Z | - |
dc.date.available | 2022-08-17T16:48:45Z | - |
dc.date.issued | 2022-09 | - |
dc.identifier.uri | http://sgc.anlis.gob.ar/handle/123456789/2450 | - |
dc.description.abstract | Encephalopathy associated with hemolytic uremic syndrome is produced by enterohemorrhagic E. coli (EHEC) infection, which releases the virulence factors Shiga toxin (Stx) and lipopolysaccharide (LPS). Neurological compromise is a poor prognosis and mortality factor of the disease, and the thalamus is one of the brain areas most frequently affected. We have previously demonstrated the effectiveness of anti-inflammatory drugs to ameliorate the deleterious effects of these toxins. However, the thalamic production of cytokines involved in pro-inflammatory processes has not yet been acknowledged. The aim of this work attempts to determine whether systemic sublethal Stx2a or co-administration of Stx2a with LPS are able to rise a proinflammatory profile accompanying alterations of the neurovascular unit in anterior and lateral ventral nuclei of the thalamus (VA-VL) and motor behavior in mice. After 4 days of treatment, Stx2a affected the lectin-bound microvasculature distribution while increasing the expression of GFAP in reactive astrocytes and producing aberrant NeuN distribution in degenerative neurons. In addition, increased swimming latency was observed in a motor behavioral test. All these alterations were heightened when Stx2a was co-administered with LPS. The expression of pro-inflammatory cytokines TNFα, INF-γ and IL-2 was detected in VA-VL. All these effects were concomitant with increased expression of the Stx receptor globotriaosylceramide (Gb3), which hints at receptor involvement in the neuroinflammatory process as a key finding of this study. In conclusion, Stx2a to Gb3 may be determinant in triggering a neuroinflammatory event, which may resemble clinical outcomes and should thus be considered in the development of preventive strategies. | es |
dc.language.iso | eng | es |
dc.relation.ispartof | Toxicon : official journal of the International Society on Toxinology | es |
dc.subject | Citocinas | es |
dc.subject | Lipopolisacáridos | es |
dc.subject | Toxinas Shiga | es |
dc.title | Cytokines expression from altered motor thalamus and behavior deficits following sublethal administration of Shiga toxin 2a involve the induction of the globotriaosylceramide receptor | es |
dc.type | Artículo | es |
dc.identifier.doi | 10.1016/j.toxicon.2022.07.003 | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | none | - |
item.openairetype | Artículo | - |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
crisitem.author.dept | Administración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS) | - |
crisitem.author.dept | Centro Nacional de Control de Calidad de Biológicos (CNCCB) | - |
crisitem.author.dept | Administración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS) | - |
crisitem.author.dept | Centro Nacional de Control de Calidad de Biológicos (CNCCB) | - |
crisitem.author.parentorg | Administración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS) | - |
crisitem.author.parentorg | Administración Nacional de Laboratorios e Institutos de Salud “Dr. Carlos G. Malbrán” (ANLIS) | - |
Appears in Collections: | Publicaciones CNCCB |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.