Gabriela A Martínez-Nava1, Eder O Méndez-Salazar2,3, Janitzia Vázquez-Mellado4, Yessica Zamudio-Cuevas5, Adriana Francisco-Balderas6, Karina Martínez-Flores5, Javier Fernández-Torres5, Carlos Lozada-Pérez7, Dafne L Guido-Gómora8, Laura E Martínez-Gómez1, Guadalupe E Jiménez-Gutiérrez1, Carlos Pineda9, Luis H Silveira10, Laura Sánchez-Chapul11, Roberto Sánchez-Sánchez12,13, María Del Carmen Camacho-Rea14, Carlos Martínez-Armenta1, Ana I Burguete-García15, Citlalli Orbe-Orihuela15, Alfredo Lagunas-Martínez15, Berenice Palacios-González2, Alberto López-Reyes16. 1. Laboratorio de Gerociencias, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Calz México-Xochimilco 289, Coapa, Arenal Tepepan, 14389, Mexico City, México. 2. Unidad de Vinculación Científica de La Facultad de Medicina UNAM-INMEGEN, Instituto Nacional de Medicina Genómica, Mexico City, México. 3. Postgraduate Program in ICES, Facultad de Química, Universidad Nacional Autónoma de México, Mexico City, Mexico. 4. Servicio de Reumatología, Hospital General de México "Dr. Eduardo Liceaga", Mexico City, México. 5. Laboratorio de Líquido Sinovial, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Mexico City, México. 6. Instituto Mexicano del Seguro Social, Mexico City, México. 7. Servicio de Reumatología, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Mexico City, México. 8. Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Mexico City, México. 9. Dirección General, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Mexico City, México. 10. Departamento de Reumatología, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City, México. 11. Laboratorio de Enfermedades Neuromusculares, División de Neurociencias Clínicas, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Mexico City, México. 12. Laboratorio de Ingeniería de Tejidos Terapia Celular y Medicina Regenerativa, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Mexico City, México. 13. Escuela de Ingeniería y Ciencias, Departamento de Bioingeniería, Instituto Tecnológico de Monterrey, Mexico City, México. 14. Departamento de Nutrición Animal, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Secretaria de Salud, Mexico City, Mexico. 15. Departamento de Epidemiología Genética, Centro de Investigaciones Sobre Enfermedades Infecciosas, Instituto Nacional de Salud Pública, Cuernavaca, México. 16. Laboratorio de Gerociencias, Instituto Nacional de Rehabilitación "Luis Guillermo Ibarra Ibarra", Calz México-Xochimilco 289, Coapa, Arenal Tepepan, 14389, Mexico City, México. allorey@yahoo.com.
Abstract
INTRODUCTION/ OBJECTIVES: Persistent hyperuricemia is a key factor in gout; however, only 13.5% of hyperuricemic individuals manifest the disease. The gut microbiota could be one of the many factors underlying this phenomenon. We aimed to assess the difference in taxonomic and predicted functional profiles of the gut microbiota between asymptomatic hyperuricemia (AH) individuals and gout patients. METHODS: The V3-V4 region of the 16S rRNA gene of the gut microbiota of AH individuals, gout patients, and controls was sequenced. Bioinformatic analyses were carried out with QIIME2 and phyloseq to determine the difference in the relative abundance of bacterial genera among the study groups. Tax4fun2 was used to predict the functional profile of the gut microbiota. RESULTS: AH individuals presented a higher abundance of butyrate- and propionate-producing bacteria than gout patients; however, the latter had more bacteria capable of producing acetate. The abundance of Prevotella genus bacteria was not significantly different between the patients but was higher than that in controls. This result was corroborated by the functional profile, in which AH individuals had less pyruvate oxidase abundance than gout patients and less abundance of an enzyme that regulates glutamate synthetase activation than controls. CONCLUSION: We observed a distinctive taxonomic profile in AH individuals characterized by a higher abundance of short-chain fatty acid-producing bacteria in comparison to those observed in gout patients. Furthermore, we provide scientific evidence that indicates that the gut microbiota of AH individuals could provide anti-inflammatory mediators, which prevent the appearance of gout flares. Key Points • AH and gout patients both have a higher abundance of Prevotella genus bacteria than controls. • AH individuals' gut microbiota had more butyrate- and propionate-producing bacteria than gout patients. • The gut microbiome of AH individuals provides anti-inflammatory mediators that could prevent gout flares.
INTRODUCTION/ OBJECTIVES: Persistent hyperuricemia is a key factor in gout; however, only 13.5% of hyperuricemic individuals manifest the disease. The gut microbiota could be one of the many factors underlying this phenomenon. We aimed to assess the difference in taxonomic and predicted functional profiles of the gut microbiota between asymptomatic hyperuricemia (AH) individuals and gout patients. METHODS: The V3-V4 region of the 16S rRNA gene of the gut microbiota of AH individuals, gout patients, and controls was sequenced. Bioinformatic analyses were carried out with QIIME2 and phyloseq to determine the difference in the relative abundance of bacterial genera among the study groups. Tax4fun2 was used to predict the functional profile of the gut microbiota. RESULTS: AH individuals presented a higher abundance of butyrate- and propionate-producing bacteria than gout patients; however, the latter had more bacteria capable of producing acetate. The abundance of Prevotella genus bacteria was not significantly different between the patients but was higher than that in controls. This result was corroborated by the functional profile, in which AH individuals had less pyruvate oxidase abundance than gout patients and less abundance of an enzyme that regulates glutamate synthetase activation than controls. CONCLUSION: We observed a distinctive taxonomic profile in AH individuals characterized by a higher abundance of short-chain fatty acid-producing bacteria in comparison to those observed in gout patients. Furthermore, we provide scientific evidence that indicates that the gut microbiota of AH individuals could provide anti-inflammatory mediators, which prevent the appearance of gout flares. Key Points • AH and gout patients both have a higher abundance of Prevotella genus bacteria than controls. • AH individuals' gut microbiota had more butyrate- and propionate-producing bacteria than gout patients. • The gut microbiome of AH individuals provides anti-inflammatory mediators that could prevent gout flares.
Authors: Maartje C P Cleophas; Tania O Crişan; Heidi Lemmers; Helga Toenhake-Dijkstra; Gianluca Fossati; Tim L Jansen; Charles A Dinarello; Mihai G Netea; Leo A B Joosten Journal: Ann Rheum Dis Date: 2015-01-14 Impact factor: 19.103
Authors: E E Blaak; E E Canfora; S Theis; G Frost; A K Groen; G Mithieux; A Nauta; K Scott; B Stahl; J van Harsselaar; R van Tol; E E Vaughan; K Verbeke Journal: Benef Microbes Date: 2020-08-31 Impact factor: 4.205
Authors: Eder Orlando Méndez-Salazar; Gabriela Angélica Martínez-Nava; Janitzia Vázquez-Mellado; Carlos S Casimiro-Soriguer; Joaquin Dopazo; Cankut Çubuk; Yessica Zamudio-Cuevas; Adriana Francisco-Balderas; Karina Martínez-Flores; Javier Fernández-Torres; Carlos Lozada-Pérez; Carlos Pineda; Austreberto Sánchez-González; Luis H Silveira; Ana I Burguete-García; Citlalli Orbe-Orihuela; Alfredo Lagunas-Martínez; Alonso Vazquez-Gomez; Alberto López-Reyes; Berenice Palacios-González Journal: Mol Med Date: 2021-05-24 Impact factor: 6.354