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Differential Expression Profiles of Orphan Nuclear Receptors (NR4A) and N-myc Downstream-Regulated Gene Family (NDRG) in Patients with Inflammatory Bowel Disease
(MDPI AG, 2026-05-26)
Fonseca-Camarillo, Gabriela
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Furuzawa-carballeda Janette
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Aguilar-León, Diana
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Barreto-Zuñiga, Rafael
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Martínez-Benítez, Braulio
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Granulomatous liver disease in a referral center in Mexico city
(Elsevier BV, 2025-07)
Ruiz-Manríquez, Jesús
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Feria-Agudelo, Sandra M.
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Olivas-Martinez, Antonio
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Martínez-Sánchez, Froylan D.
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Azamar-Llamas, Daniel
Introduction and Objectives: Up to 15 % of liver biopsies may reveal granulomas. The underlying causes vary geographically, with marked differences between high- and low-middle-income countries. No studies have examined the etiology of granulomatous liver disease (GLD) in Mexico. This study aims to describe the etiologic profile and clinical outcomes of patients diagnosed with GLD at a tertiary care center in Mexico. Materials and Methods: Retrospective cohort study of patients diagnosed with GLD by liver biopsy between 2001 and 2017. Results: We identified 133 patients with GLD. The most common causes were infectious diseases (36.1 %, n = 48; including 22 mycobacterial infections), foreign body reactions (21.1 %, n = 28), and autoimmune disorders (15.0 %, n = 20). The overall 6-month survival probability was 90.9 % (95 % confidence interval [CI], 86–95 %), declining to 87.5 % (95 % CI, 82–93 %) at 12 months. Patients with autoimmune etiologies had the best prognosis (100 % survival at 6 and 12 months). In contrast, patients with neoplastic GLD had the poorest outcomes, with survival probabilities of 72.7 % (95 % CI, 50.6–100 %) at 6 months and 63.6 % (95 % CI, 40.7–99.5 %) at 12 months. Patients with idiopathic GLD had a favorable short-term prognosis, with a 12-month survival probability of 92 %. Conclusions: In this cohort, infectious diseases were the most common cause of GLD. Prognosis varied by etiology, with idiopathic cases showing favorable short-term outcomes and neoplastic cases exhibiting poor survival rates. ©The authors ©Annals of Hepatology ©Elsevier.
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Protective role of ABCC drug subfamily resistance transporters (ABCC1-7) in intestinal inflammation
(Springer Nature, 2025)
Fonseca-Camarillo, Gabriela
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Furuzawa-Carballeda, Janette
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Miguel-Cruz, Erika
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Barreto-Zuñiga, Rafel
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Martínez-Benítez, Braulio
The ABCC subfamily contains thirteen members. Nine of these transporters are called multidrug resistance proteins (MRPs). The MRPs have been associated with developing ulcerative colitis (UC). This study aimed to evaluate the ABCC expression in UC patients and its role in a dextran sulfate sodium (DSS)-induced colitis mice model under 5-aminosalicylates or methylprednisolone treatment and compared with control without inflammation. DSS-induced colitis mice were treated with 5-aminosalicylates (50 mg/kg 24 h) or methylprednisolone (2 mg/kg 24 h). Human rectal biopsies were obtained from UC patients. The abcc-relative mRNA levels and protein expression were determined by RT-PCR and immunohistochemistry. abcc4, abcc5, and abcc6 mRNA levels were significantly increased in DSS-induced colitis compared to the other groups. The 5-aminosalicylate treatment dramatically increased the abcc2 and abcc3 mRNA levels vs. control. Methylprednisolone treatment increased abcc1 vs. DSS-induced colitis and colitis treated with 5-aminosalicylate. Immunohistochemical analysis revealed down-regulation of ABCC1/ABCC2/ABCC5/ABCC7 in mice colitis vs. control. Treatment with 5-aminosalicylate restored ABCC5 levels, while methylprednisolone restored ABCC2/ABCC5/ABCC7 in colitis mice at similar control levels. Relative mRNA levels of mrp1-5 were increased in active UC patients vs. control. ABCC2/ABCC4/ABCC7 were conspicuously expressed in the mucosa of 5-aminosalicylate and/or methylprednisolone-treated UC patients, while ABCC2/ABCC4/ABCC5/ABCC7 in submucosa, ABCC1/ABCC5/ABCC7 in muscular, and ABCC1/ABCC4/ABCC5/ABCC7 in serosa were expressed vs. controls. This is the first report about the differential up-regulation of the ABCC subfamily gene and protein expression in DSS-induced colitis under aminosalicylates or methylprednisolone treatment. ©The authors ©Springer.
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Protective Role of Selenium-Binding Protein 1 (SELENBP1) in Patients with Ulcerative Colitis
(MDPI, 2024)
Fonseca-Camarillo, Gabriela
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Furuzawa-Carballeda, Janette
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Priego-Ranero, Ángel A.
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Barreto-Zúñiga, Rafael
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Martínez-Benítez, Braulio
Background: The expression of selenium-binding protein 1 (SELENBP1), a molecule responsible for the absorption of selenium in the colon, is crucial for its immunoregulatory effect, but this phenomenon has not been studied in patients with UC. The present study aimed to determine the clinical outcome of SELENBP1 expression in colonic tissue from patients with UC. Methods: The relative mRNA expression of SELENBP1 was analyzed in 34 patients with UC and 20 controls. Statistical analyses were performed with SPSS 19. Results: SELENBP1 gene expression was significantly lower in patients with active UC than those with UC in remission (p = 0.003) and within the controls (p = 0.04). Overexpression of the SELENBP1 gene was associated with a more benign clinical course characterized by initial activity and more than two years of prolonged remission (OR 23.7, p = 0.003) and an intermittent clinical course (OR 47.5, p = 0.001), mild histological activity (OR 0.11; 95% CI: 1.00–1.41, p = 0.05) and severe histological activity (OR 0.08, 95% CI: 0.008–0.866, p = 0.02). SELENBP1-positive cells were found mainly in the submucosa’s inflammatory infiltrate and muscular and adventitia’s internal layers from patients with active UC compared to those in the control group (p ≤ 0.001). Conclusions: The upregulation of SELENBP1 was associated with a benign clinical course of UC. This is the first report suggesting the immunoregulatory role of SELENBP1 in patients with UC. ©The authors ©MDPI
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