RESUMEN
Gastrointestinal mucosal surface is frequently under challenge due to it's the large surface area and most common entry of microbes. IL-37, an anti-inflammatory cytokine, regulates local and systemic host immunity. H. pylori infection leads to the inhibition of IL-37 in the gastric mucosa, contributing to heightened mucosal inflammation and destruction, thereby facilitating increased proliferation of H. pylori. Food allergy, due to immune dysregulation, also contribute to GI injury. On the other hand, elevated levels of IL-37 observed in gastric cancer patients align with reduced host immunity at the cellular and humoral levels, indicating that IL-37 may contribute to the development of gastric cancer via suppressing pro-inflammatory responses. While IL-37 provides protection in an IBD animal model, the detection of highly produced IL-37 in IBD patients suggests a stage-dependent role, being protective in acute inflammation but potentially exacerbates the development of IBD in chronic conditions. Moreover, elevated colonic IL-37 in CRC correlates with overall survival time and disease time, indicating a protective role for IL-37 in CRC. The differential regulation and expression of IL-37 between upper- and lower-GI organs may be attributed to variations in the microbial flora. This information suggests that IL-37 could be a potential therapeutic agent, depending on the stage and location.
Asunto(s)
Enfermedades Gastrointestinales , Interleucina-1 , Humanos , Interleucina-1/metabolismo , Animales , Enfermedades Gastrointestinales/inmunología , Enfermedades Gastrointestinales/metabolismo , Infecciones por Helicobacter/inmunología , Infecciones por Helicobacter/metabolismo , Mucosa Gástrica/metabolismo , Mucosa Gástrica/inmunología , Mucosa Gástrica/microbiología , Helicobacter pylori/inmunología , Microbioma Gastrointestinal/inmunologíaRESUMEN
IL-38, an anti-inflammatory cytokine, is a key regulator of homeostasis in host immunity. Intestinal immunity plays a critical role in defence against pathogenic invasion, as it is the largest surface organ and the most common entry point for micro-organisms. Dysregulated IL-38 activity is observed in several autoimmune diseases including systemic lupus erythematosus and atherosclerosis. The protective role of IL-38 is well illustrated in experimental colitis models, showing significantly worse colitis in IL-38 deficient mice, compared to wildtype mice. Moreover, exogenous IL-38 has been shown to ameliorate experimental colitis. Surprisingly, upregulated IL-38 is detected in inflamed tissue from inflammatory bowel disease patients, consistent with increased circulating cytokine levels, demonstrating the complex nature of host immunity in vivo. However, colonic IL-38 is significantly reduced in malignant tissues from patients with colorectal cancer (CRC), compared to adjacent non-cancerous tissue. Additionally, IL-38 expression in CRC correlates with 5-year survival, tumour size and differentiation, suggesting IL-38 plays a protective role during the development of CRC. IL-38 is also an independent biomarker for the prognosis of CRC, offering useful information in the management of CRC. Taken together, these data demonstrate the role of IL-38 in the maintenance of normal intestinal mucosal homeostasis, but that dysregulation of IL-38 contributes to initiation of chronic inflammatory bowel disease (resulting from persistent local inflammation), and that IL-38 provides protection during the development of colorectal cancer. Such data provide useful information for the development of novel therapeutic targets in the management of intestinal diseases for more precise medicine.
Asunto(s)
Colitis , Neoplasias Colorrectales , Enfermedades Inflamatorias del Intestino , Ratones , Animales , Citocinas , Neoplasias Colorrectales/patologíaRESUMEN
Kidney fibrosis is usually the final manifestation of a wide variety of renal diseases. Recent years, research reported that long non-coding RNAs (lncRNAs) played important roles in a variety of human diseases. However, the role and underlying mechanisms of lncRNAs in kidney fibrosis were complicated and largely unclear. In our study, we constructed the cell model of renal fibrosis in HK2 cells using transforming growth factor ß1 (TGF-ß1) and found that lncRNA maternally expressed gene 3 (MEG3) was downregulated in TGF-ß1-induced renal fibrosis. We then found that overexpressed MEG3 inhibited the TGF-ß1-induced promotion of epithelial-mesenchymal transition, cell viability, and proliferation. Furthermore, we demonstrated that DNA methyltransferases 1 (DNMT1) regulated the MEG3 expression by altering the CpGs methylation level of MEG3 promoter in TGF-ß1-induced renal fibrosis. In addition, we further revealed that miR-185 could regulate the DNMT1 expression and thus, modulate the MEG3 in TGF-ß1-induced renal fibrosis. Ultimately, our study illustrated that the modulation of the miR-185/ DNMT1/ MEG3 pathway exerted important roles in TGF-ß1-induced renal fibrosis. In summary, our finding displayed a novel regulatory mechanism for TGF-ß1-induced renal fibrosis, which provided a new potential therapeutic target for renal fibrosis.
Asunto(s)
ADN (Citosina-5-)-Metiltransferasa 1/metabolismo , Riñón/patología , MicroARNs/fisiología , ARN Largo no Codificante/metabolismo , Línea Celular , Proliferación Celular , Supervivencia Celular , Transición Epitelial-Mesenquimal , Fibrosis , Humanos , Factor de Crecimiento Transformador beta1/químicaRESUMEN
Irritable bowel syndrome (IBS) is a functional intestinal disease characterized by abdominal pain or discomfort and altered bowel habits. It has drawn great attention because of its high prevalence, reoccurring symptoms, and severe influence on patients' lives. Many clinical studies have demonstrated the efficacy of acupuncture-moxibustion in treating IBS. Increasing attention has been paid to research regarding the action mechanisms of acupuncture-moxibustion for IBS, and the adoption of modern techniques has achieved some progress. This article reviews the latest advances among action mechanism studies from the perspectives of gastrointestinal motility, visceral hypersensitivity, the brain-gut axis, the neuroendocrine system, and the immune system. It is shown that acupuncture-moxibustion can effectively regulate the above items, and thus, this treatment should have a high efficacy in the treatment of IBS. This article also identifies existing problems in current mechanism research and raises several ideas for future studies. Further revelations regarding these action mechanisms will promote the application of acupuncture-moxibustion in treating IBS.
Asunto(s)
Terapia por Acupuntura , Síndrome del Colon Irritable/terapia , Moxibustión , Animales , Encéfalo/fisiología , Células Endocrinas/fisiología , Motilidad Gastrointestinal , Humanos , Hipersensibilidad , Intestinos/fisiopatología , Síndrome del Colon Irritable/etiología , Síndrome del Colon Irritable/fisiopatología , Neuronas/metabolismo , Neuronas/fisiología , Sistemas NeurosecretoresRESUMEN
Urinary retention is a frequent-encountered complication after gynaecological surgery. It affects the postoperative recovery and decreases the life quality of patients. In recent years, extensive researches on causes and treatments of postoperative urinary retention are carried out in clinic. And it is approved that acupuncture treatment, which includes body needling, moxibustion, combination of acupuncture and moxibustion, acupoint injection and medication plasters, has reliable effects and less side-effects. Acupuncture treatment on postoperative urinary retention keeps developing and innovating. And it is held to have better effect when compare with western medicine.