Recently, accumulating evidence has suggested that gut microbiota may be involved in the occurrence and development of ankylosing spondylitis (AS). It has been suggested that rifaximin have the ability to modulate the gut bacterial communities, prevent inflammatory response, and modulate gut barrier function. The goal of this work is to evaluate the protective effects of rifaximin in fighting AS and to elucidate the potential underlying mechanism. Rifaximin were administered to the proteoglycan (PG)-induced AS mice for 4 consecutive weeks. The disease severity was measured with the clinical and histological of arthritis and spondylitis. Intestinal histopathological, pro-inflammatory cytokine levels and the intestinal mucosal barrier were evaluated. Then, western blot was performed to explore the toll-like receptor 4 (TLR-4) signal transducer and NF-κB expression. Stool samples were collected to analyze the differences in the gut microbiota via next-generation sequencing of 16S rDNA. We found that rifaximin significantly reduced the severity of AS and resulted in down-regulation of inflammatory factors, such as TNF-α, IL-6, IL-17A, and IL-23. Meanwhile, rifaximin prevented ileum histological alterations, restored intestinal barrier function and inhibited TLR-4/NF-κB signaling pathway activation. Rifaximin also changed the gut microbiota composition with increased Bacteroidetes/Firmicutes phylum ratio, as well as selectively promoting some probiotic populations, including Lactobacillales . Our results suggest that rifaximin suppressed progression of AS and regulated gut microbiota in AS mice. Rifaximin might be useful as a novel treatment for AS.
Ankylosing spondylitis is a chronic, progressive disease, and its treatment is relevant to the gut microbiota. Anti‐tumor necrosis factor‐alpha (anti‐TNF‐α) therapy alters the gut microbiota in many diseases, including inflammatory bowel disease. However, little is known about the effect of TNF‐α blocker treatment on the gut microbiota in ankylosing spondylitis. Herein, the effect of a TNF‐α blocker on the gut microbiota in proteoglycan‐induced arthritis was investigated. Proteoglycan‐induced mice were treated with an rhTNFR:Fc solution of etanercept (5 µg/g) for 4 weeks. rhTNFR:Fc treatment attenuated the arthritis incidence and severity of arthritis in the proteoglycan‐induced mice and decreased inflammation in the ankle joints and ameliorated ileal tissue destruction. Moreover, high gut permeability occurred, and zonula occludens‐1 and occludin protein levels were reduced in proteoglycan‐induced mice. These levels were significantly restored by the administration of rhTNFR:Fc. The serum TNF‐α and IL‐17 levels were also decreased. In addition, flora analysis via 16S rDNA high‐throughput sequencing revealed that rhTNFR:Fc treatment restored the gut microbiota composition to a composition similar to that in control mice. In conclusion, anti‐TNF‐α therapy attenuated proteoglycan‐induced arthritis progression and modulated the gut microbiota and intestinal barrier function. These results provide new insights for anti‐TNF‐α therapy strategies via regulating the gut microbiota in ankylosing spondylitis.
Background: The detailed structure of the lumbar intervertebral foramina has been wellstudied. Nevertheless, detailed descriptions of branches of the intervertebral vein (IV) through the lumbar intervertebral foramina are lacking. Objectives: This study aimed to provide an anatomical basis for invasive treatment targeting the branches of the IV using an approach through the lumbar intervertebral foramina, particularly for the purposes of transforaminal epidural steroid injection. Study Design: This research involved a dissection-based study of 10 embalmed human cadavers. Setting: The research took place at The Third Affiliated Hospital of Southern Medical University. Methods: One hundred lumbar intervertebral foramina from 10 embalmed cadavers were studied. Branches of the IV in the intervertebral foramina were observed. The length and diameter of the veins were measured using a Vernier caliper. Results: At a rate of 100%, branches of the IV were observed in the 100 lumbar foramina examined in our study. The following 4 types of branches of the IV were routinely found: Type I in 27 (27%) of the IV foramina, in which a superior branch of the IV ran along the inferior margin of the vertebral pedicle; Type II in 18 (18%) of the intervertebral foramina, in which an inferior branch of the IV ran along the superior margin of the inferior vertebral pedicle; Type III in 41 (41%) of the intervertebral foramina, in which the IV was divided into a superior and inferior branch; and Type IV in 14 (14%) of the intervertebral foramina, in which the IV was divided into 2 superior branches and an inferior branch. Limitations: The greatest weakness of this study is that it lacks actual clinical verification. Future clinical trials are expected to contribute more objective data concerning the IV branches. Due to the relative changes in vascular position during dissection, the relevant data warrant improvement. Conclusions: The lumbar IVs are an important part of the anatomical structure of the intervertebral foramina. Adequate knowledge of the IV may be of clinical importance to physicians performing transforaminal epidural steroid injection. Key words: Clinical anatomy, intervertebral veins, lumbar vertebra, Kambin’s triangle, safe triangle, intervertebral foramina, vertebral venous system, inadvertent injection, transforaminal epidural steroid injection
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