Activation of pathogenic Th17 lymphocytes induce hypertension after high-fructose intake. Immune activation plays an important role in the development of hypertension whereas immune tolerance does in the protection against hypertension. ABSTRACT Objectives: High-salt or high-fructose intakes are risk factors for hypertension via oxidative stress and inflammation. T helper (Th)17 lymphocytes play an important role in the development of hypertension. We tested the hypothesis that activation of pathogenic Th17 lymphocytes induces hypertension after high-fructose intake in Dahl salt-sensitive (SS) but not Dahl salt-resistant (SR) rats. Methods: Eight-week-old male SS and SR rats were offered 20% fructose solution or tap water only for 4 weeks. Systolic blood pressure was measured by the tail-cuff method. T lymphocytes (Th17 and T regulatory (Treg)) profiling was determined via flow cytometry. The expression of Th17 -related (interleukin (IL)-17A, IL-17RA,IL-23R and retinoic acid receptor-related orphan receptor (ROR) γt) and Treg-related (IL-10, CD25, forkhead box (Fox)P3, and TGF-ß) factors were measured via ELISA or qRT-PCR. Th17 lymphocytes isolated from high fructose-fed SS rats were intraperitoneally injected into recipient SS and SR rats. Moreover, recombinant IL-23 protein was subcutaneously injected into SS and SR rats to induce hypertension. Results: High-fructose intake induced hypertension via the activation of pathogenic Th17 lymphocytes in SS but not SR rats. Injection of activated Th17 lymphocytes isolated from fructosefed SS rats induced hypertension via increase of serum IL-17A in only recipient SS rat. In addition, injection of IL-23 induced hypertension via activation of pathogenic Th17 lymphocytes in only SS rats.Conclusion: Activation of pathogenic Th17 lymphocytes induces hypertension after high-fructose intake in SS but not SR rats. These results implicate that immunologic tolerance plays an important role in the protection against hypertension in SR.
Allergic bronchopulmonary aspergillosis (ABPA) is a pulmonary disease with small prevalence. Exposure to aspergillus mold causes immunologic hypersensitivity and may cause ranges of symptoms from minimal to detrimental outcomes. Diagnosing and treating the disease before the development of bronchiectasis may save the patient from poor outcomes. This report presents a case of recurrent ABPA without any symptom of asthma, which impeded the correct diagnosis even after numerous hospitalizations.
Introduction: Although both glucose and fructose are hexoses, their catabolism is quite different: the catabolism of fructose is initiated by ketohexokinase and is not regulated by negative feedback, which results in oxidative stress. Objective: We hypothesized that fructose impairs endothelium-dependent relaxation via oxidative stress in rat aortic rings. Methods: Sprague-Dawley rats were offered 20% fructose solution or tap water for 2 weeks, after which vascular reactivity was measured in isolated aortic rings. In a separate experiment, vascular reactivity was measured after acute exposure to ∼10 mM fructose in isolated aortic rings from untreated rats. Results: Although high-fructose intake statistically significantly increased blood pressure and body weight, it did not affect contraction and relaxation in aortic rings. The substitution of fructose for glucose in Krebs solution inhibited vascular relaxation in aortic rings, which was abolished by pretreatment with antioxidants. Decreasing the glucose concentration in Krebs solution inhibited vascular relaxation , whereas decreasing the fructose concentration in Krebs solution improved vascular relaxation in the aortic rings. Pretreatment with antioxidants improved the vascular relaxation in Krebs solution with fructose substituted for glucose. Conclusions: These results indicate that fructose impairs endothelium-dependent relaxation via oxidative stress in isolated rat aortic rings.
Background/Aims: Hip fracture and acute exacerbation of chronic obstructive pulmonary disease (AE-COPD) could increase mortality in patients with COPD. There are no data on the relationship between AE-COPD and hip fracture, which may significantly affect the prognosis of patients with COPD. Therefore, we conducted this study to determine the effects of AE-COPD on hip fractures in patients with COPD. Methods: This retrospective, nested, case-control study included 253,471 patients with COPD (≥ 40 years of age) identified from the Korea National Health Insurance Service-National Health Screening Cohort (NHIS-HEALS) from 2002 to 2015. Among 176,598 patients with COPD, 1,415 patients with hip fractures were identified. Each case was matched to one control for age (within 10 years), sex, and year of COPD diagnosis. We estimated the adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for hip fractures associated with AE-COPD using conditional logistic regression analysis, adjusting for underlying diseases and smoking history. Results: In patients with AE-COPD, the risk of hip fracture was 2.50 times higher, regardless of systemic corticosteroid use and underlying disease (aOR, 2.50; 95% CI, 1.67 to 3.75). The risk of hip fracture increased if there was one episode of AE in the year before hip fractures (aOR, 2.25; 95% CI, 1.66 to 3.05). Moreover, the risk of hip fracture also increased in patients with more than two episodes of AE the year before hip fractures (aOR, 2.57; 95% CI, 1.61 to 4.10). Conclusions: AE-COPD increases the risk of hip fracture regardless of underlying diseases, including osteoporosis, and treatment with systemic corticosteroids.
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