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The detrimental effects of lipopolysaccharideinduced neuroinflammation on adult hippocampal neurogenesis depend on the duration of the pro-inflammatory response

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Neural Regeneration Research 2019年第5期14卷 817-825页

作者： Martha Pérez-domínguez Evangelina ávila-Mu?oz eduardo domínguez-rivas Angélica Zepeda Departamento de Medicina Genómica y Toxicología Ambiental Instituto de Investigaciones Biomédicas.Universidad Nacional Autónoma de MéxicoCDMX

Adult hippocampal neurogenesis is a finely tuned process regulated by extrinsic factors. Neuroinflammation is a hallmark of several pathological conditions underlying dysregulation of neurogenesis. In animal models, lipopolysaccharide(LPS)-induced neuroinflammation leads to a neurogenic decrease mainly associated to the early inflammatory response. However, it is not well understood how the neuroinflammatory response progresses over time and if neurogenesis continues to be diminished during the late neuroinflammatory response. Moreover, it is unknown if repeated intermittent administration of LPS along time induces a greater reduction in neurogenesis. We administered one single intraperitoneal injection of LPS or saline or four repeated injections(one per week) of LPS or saline to young-adult mice. A cohort of new cells was labeled with three 5-bromo-2-deoxyuridine injections(one per day) 4 days after the last LPS injection. We evaluated systemic and neuroinflammation-associated parameters and compared the effects of the late neuroinflammatory response on neurogenesis induced by each protocol. Our results show that 1) a single LPS injection leads to a late pro-inflammatory response characterized by microglial activation, moderate astrocytic reaction and increased interleukin-6 levels. This response correlates in time with decreased neurogenesis and 2) a repeated intermittent injection of LPS does not elicit a late pro-inflammatory response although activated microglia persists. The latter profile is not accompanied by a continued longterm hippocampal neurogenic decrease. Hereby, we provide evidence that the neuroinflammatory response is a dynamic process that progresses in a milieu-dependent manner and does not necessarily lead to a neurogenic decrease, highlighting the complex interaction between the immune system and neurogenesis.

关键词： dentate gyrus subgranular zone inflammation microglia astrocytes IL-6 cytokines cell proliferation neural progenitor cells immature neurons long-term short-term adult hippocampal neurogenesis

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Severe <i>Citrus tristeza virus</i>Isolates from Eastern Mexico Are Related to the T36 Genotype Group

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American Journal of Plant Sciences 2020年第10期11卷 1521-1532页

作者： Patricia rivas-Valencia Santiago domínguez-Monge Ricardo Santillán-Mendoza Emiliano Loeza-Kuk Oscar Pérez-Hernández Cynthia G. Rodríguez-Quibrera Claudia Lomas-Barrié Instituto Nacional de Investigaciones Forestales Agrícolas y Pecuarias-Campo Experimental Valle de México Carretera Los Reyes-Texcoco km 13.5 Coatlinchán Texcoco México Instituto Nacional de Investigaciones Forestales Agrícolas y Pecuarias-Campo Experimental Ixtacuaco Carretera Martínez de la Tor-re-Tlapacoyan km 4.5 Tlapacoyan Veracruz México Instituto Nacional de Investigaciones Forestales Agrícolas y Pecuarias-Campo Experimental Ixtacuaco Carretera Martínez de la Torre-Tlapacoyan km 4.5 Tlapacoyan Veracruz México Instituto Nacional de Investigaciones Forestales Agrícolas y Pecuarias-Campo Experimental Mocochá Carretera Mérida-Motul km 25 Mocochá Yucatán México School of Agricultural Sciences Northwest Missouri State University Maryville USA

Citrus tristeza virus (CTV) outbreaks have been reported in the main citrus growing region of Mexico in the past four years. Recently, in eastern Mexico (the major citrus-growing region in the country), severe CTV isolates have been detected. However, the molecular identity of observed isolates remains unestablished. This research was undertaken to elucidate the molecular characterization of CTV populations spreading in this region and to compare it with phylogeny of existing isolates. Genotyping of 32 collected isolates was performed using reverse-transcription polymerase chain reaction (RT-PCR) with sequence analysis of the coat protein (CP) gene, putatively associated with pathogenicity. This protein is a 25 kDa major capsid protein, which forms a long virion body coating 95% of the particle length. A comparative sequence analysis was performed using CTV sequences from different geographical origins already published and deposited in the GenBank databases. Phylogenetic analysis showed that the degree of sequence divergence among isolates correlated with their pathogenicity. Based on the sequencing results, the collected isolates were categorizedn as mild or severe phylogenetic clusters

关键词： CTV Epidemiology Severe Isolates Stem Pitting Quick Decline Coat Protein Gene

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Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection

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Cellular & Molecular Immunology 2021年第9期18卷 2128-2139页

作者： Alberto Pérez-Gómez Joana Vitallé Carmen Gasca-Capote Alicia Gutierrez-Valencia María Trujillo-Rodriguez Ana Serna-Gallego Esperanza Muñoz-Muela María de los Reyes Jiménez-Leon Mohamed Rafii-El-Idrissi Benhnia Inmaculada rivas-Jeremias Cesar Sotomayor Cristina Roca-Oporto Nuria Espinosa Carmen Infante-domínguez Juan Carlos Crespo-rivas Alberto Fernández-Villar Alexandre Pérez-González Luis Fernando López-Cortés Eva Poveda Ezequiel Ruiz-Mateos JoséMiguel Cisneros Sonsoles Salto-Alejandre Judith Berastegui-Cabrera Pedro Camacho-Martínez Carmen Infante-domínguez Marta Carretero-Ledesma Juan Carlos Crespo-rivas eduardo Márquez JoséManuel Lomas Claudio Bueno Rosario Amaya JoséAntonio Lepe Jerónimo Pachón Elisa Cordero Javier Sánchez-Céspedes Manuela Aguilar-Guisado Almudena Aguilera Clara Aguilera Teresa Aldabo-Pallas Verónica Alfaro-Lara Cristina Amodeo Javier Ampuero María Dolores Avilés Maribel Asensio Bosco Barón-Franco Lydia Barrera-Pulido Rafael Bellido-Alba Máximo Bernabeu-Wittel Candela Caballero-Eraso Macarena Cabrera Enrique Calderón Jesús Carbajal-Guerrero Manuela Cid-Cumplido Yael Corcia-Palomo Juan Delgado Antonio domínguez-Petit Alejandro Deniz Reginal Dusseck-Brutus Ana Escoresca-Ortega Fátima Espinosa Nuria Espinosa Michelle Espinoza Carmen Ferrándiz-Millón Marta Ferrer Teresa Ferrer Ignacio Gallego-Texeira Rosa Gámez-Mancera Emilio García Horacio García-Delgado Manuel García-Gutiérrez María Luisa Gascón-Castillo Aurora González-Estrada Demetrio González Carmen Gómez-González Rocío González-León Carmen Grande-Cabrerizo Sonia Gutiérrez Carlos Hernández-Quiles Inmaculada Concepción Herrera-Melero Marta Herrero-Romero Luis Jara Carlos Jiménez-Juan Silvia Jiménez-Jorge Mercedes Jiménez-Sánchez Julia Lanseros-Tenllado Carmina López Isabel López Álvaro López-Barrios Luis F.López-Cortés Rafael Luque-Márquez Daniel Macías-García Guillermo Martín-Gutiérrez Luis Martín-Villén JoséMolina Aurora Morillo María Dolores Navarro-Amuedo Dolores Nieto-Martín Francisco Ortega María Paniagua-García Amelia Peña-Rodríguez E Clinical Unit of Infectious Diseases Microbiology and Preventive MedicineInstitute of Biomedicine of Seville(IBiS)Virgen del Rocío University HospitalCSICUniversity of SevilleSevilleSpain Department of Medical Biochemistry Molecular Biologyand ImmunologySchool of MedicineUniversity of SevilleSevilleSpain Pneumology Service Galicia Sur Health Research Instituto(IIS Galicia Sur)SERGAS-UVigoVigoSpain Infectious Diseases Unit Department of Internal MedicineComplexo HospitalarioUniversitario de VigoIIS Galicia SurSERGAS-UVigoVigoSpain Group of Virology and Pathogenesis Galicia Sur Health Research Institute(IIS Galicia Sur)-Complexo Hospitalario Universitario de VigoSERGAS-UVigoVigoSpain Unit of Infectious Diseases Microbiologyand Preventive MedicineVirgen del Rocío University HospitalSevilleSpain Institute of Biomedicine of Seville(IBiS) Virgen del Rocío University Hospital/CSIC/University of SevilleSevilleSpain Medico-Surgical Unit of Respiratory Diseases Virgen del Rocío University HospitalSevilleSpain Unit of Emergencies Virgen del Rocío University HospitalSevilleSpain Intensive Care Unit Virgen del Rocío University HospitalSevilleSpain Department of Medicine University of SevilleSevilleSpain Cardiology and Cardiovascular Surgery Unit Virgen del Rocío University HospitalSevilleSpain Rheumatology Unit Virgen del Rocío University HospitalSevilleSpain Internal Medicine Unit Virgen del Rocío University HospitalSevilleSpain Digestive and Hepatobiliary Unit Virgen del Rocío University HospitalSevilleSpain Neurology and Clinical Neurophysiology Unit Virgen del Rocío University HospitalSevilleSpain Endocrinology and Nutrition Unit Virgen del Rocío University HospitalSevilleSpain Urology and Nephrology Unit Virgen del Rocío University HospitalSevilleSpain Unit of Clinical Investigation and Clinical Trials Virgen del Rocío University HospitalSevilleSpain

Severe Acute Respiratory Syndrome Coronavirus(SARS-CoV)-2 infection induces an exacerbated inflammation driven by innate immunity components.Dendritic cells(DCs)play a key role in the defense against viral infections,for instance plasmacytoid DCs(pDCs),have the capacity to produce vast amounts of interferon-alpha(IFN-α).In COVID-19 there is a deficit in DC numbers and IFN-αproduction,which has been associated with disease severity.In this work,we described that in addition to the DC deficiency,several DC activation and homing markers were altered in acute COVID-19 patients,which were associated with multiple inflammatory markers.Remarkably,previously hospitalized and nonhospitalized patients remained with decreased numbers of CD1c+myeloid DCs and pDCs seven months after SARS-CoV-2 infection.Moreover,the expression of DC markers such as CD86 and CD4 were only restored in previously nonhospitalized patients,while no restoration of integrinβ7 and indoleamine 2,3-dyoxigenase(IDO)levels were observed.These findings contribute to a better understanding of the immunological sequelae of COVID-19.

关键词： SARS-CoV-2 COVID-19 Dendritic cell Long-COVID

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