The impact of short-chain fatty acid–producing bacteria of the gut microbiota in hyperuricemia and gout diagnosis

Martínez‐Nava, Gabriela Angélica; Méndez-Salazar, Eder Orlando; Vázquez‐Mellado, Janitzia; Zamudio-Cuevas, Yessica; Francisco-Balderas, Adriana; Martínez-Flores, Karina; Fernández‐Torres, Javier; Lozada, Carlos; Guido-Gómora, Dafne L.; Martínez-Gómez, Laura E.; Jiménez-Gutiérrez, Guadalupe Elizabeth; Pineda, Carlos; Silveira, Luis H.; Sánchez-Chapul, Laura; Sánchez-Sánchez, Roberto; Camacho-Rea, María del Carmen; Martínez-Armenta, Carlos; Burguete-García, Ana I.; Orbe-Orihuela, Citlalli; Lagunas‐Martínez, Alfredo; Palacios‐González, Berenice; López‐Reyes, Alberto

doi:10.1007/s10067-022-06392-9

Cited by 4 publications

(2 citation statements)

References 43 publications

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“…The paper by Martinez-Nava [32] evaluated the differences between taxonomic profiles by sequencing of the V3-V4 region of the 16S rRNA gene in the intestinal microbiota, and it predicted functional profiles of the intestinal microbiota in individuals with asymptomatic hyperuricemia and 162 people, including patients with gout.…”

Section: Clinical Studiesmentioning

confidence: 99%

Reassessing Gout Management through the Lens of Gut Microbiota

Demarquoy,

Dehmej

2024

Applied Microbiology

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Gout, recognized as the most common form of inflammatory arthritis, arises from the accumulation of uric acid crystals, leading to intense pain, particularly in the big toe. This condition has traditionally been associated with the overproduction or reduced clearance of uric acid. Recent studies, however, have underscored the significant role of the gut microbiota in uric acid metabolism, impacting both its production and elimination. This emerging understanding suggests that maintaining gut health could offer innovative approaches to treating gout, complementing traditional dietary and pharmacological interventions. It highlights the potential of probiotics or microbiome-based therapies, indicating a future where treatments are tailored to an individual’s microbiome. This offers a fresh perspective on gout management and underscores the broader influence of the microbiota on health and disease.

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Section: Clinical Studiesmentioning

confidence: 99%

Reassessing Gout Management through the Lens of Gut Microbiota

Demarquoy,

Dehmej

2024

Applied Microbiology

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“…Our results support our hypothesis, as mice treated with GPLG-094 (butyrate GPR43 receptor inhibitor) showed a reduction in the anti-inflammatory and antioxidant effect of Lr. In fact, some authors have evidenced that the GPR43 receptor on immune cells is involved in diverse inflammatory conditions, such as the secretion of IL-6 from macrophages exposed to SARS-CoV-2 membrane glycoprotein [58], atherosclerotic inflammation [59], gout [60], pneumoniae infection [61], diabetes [62], adipose tissue M2-type macrophages [63], and acute lung injury [64]. Our findings add to the results of these authors, as in vivo inhibition of the GPR43 receptor decreased the Lr effect on pro-inflammatory mediators TNF-α, IL-1β, IL-6, GM-CSF, and TSLP as well as the transcription factor NF-κB, all of which are involved with the chronicity of COPD.…”

Section: Gpr43 Receptor Inhibitor Partially Attenuates Effect On In V...mentioning

confidence: 99%

Involvement of GPR43 Receptor in Effect of Lacticaseibacillus rhamnosus on Murine Steroid Resistant Chronic Obstructive Pulmonary Disease: Relevance to Pro-Inflammatory Mediators and Oxidative Stress in Human Macrophages

Sá,

Olímpio,

Vasconcelos

et al. 2024

Nutrients

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Background: Cytokine storm and oxidative stress are present in chronic obstructive pulmonary disease (COPD). Individuals with COPD present high levels of NF-κB-associated cytokines and pro-oxidant agents as well as low levels of Nrf2-associated antioxidants. This condition creates a steroid-resistant inflammatory microenvironment. Lacticaseibacillus rhamnosus (Lr) is a known anti-cytokine in lung diseases; however, the effect of Lr on lung inflammation and oxidative stress in steroid-resistant COPD mice remains unknown. Objective: Thus, we investigated the Lr effect on lung inflammation and oxidative stress in mice and macrophages exposed to cigarette smoke extract (CSE) and unresponsive to steroids. Methods: Mice and macrophages received dexamethasone or GLPG-094 (a GPR43 inhibitor), and only the macrophages received butyrate (but), all treatments being given before CSE. Lung inflammation was evaluated from the leukocyte population, airway remodeling, cytokines, and NF-κB. Oxidative stress disturbance was measured from ROS, 8-isoprostane, NADPH oxidase, TBARS, SOD, catalase, HO-1, and Nrf2. Results: Lr attenuated cellularity, mucus, collagen, cytokines, ROS, 8-isoprostane, NADPH oxidase, and TBARS. Otherwise, SOD, catalase, HO-1, and Nrf2 were upregulated in Lr-treated COPD mice. Anti-cytokine and antioxidant effects of butyrate also occurred in CSE-exposed macrophages. GLPG-094 rendered Lr and butyrate less effective. Conclusions: Lr attenuates lung inflammation and oxidative stress in COPD mice, suggesting the presence of a GPR43 receptor-dependent mechanism also found in macrophages.

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