The recently discovered IL-33 as an IL-1 cytokine family member has been proved to be specifically released from osteonecrotic bones. We aimed to investigate the potential role of IL-33 in the development of osteonecrosis of femoral head (ONFH). Forty patients diagnosed with ONFH and forty age-, sex-, and body mass index- (BMI-) matched healthy subjects were included in this prospective study between March 2016 and September 2016. A commercially available ELISA kit was used to test the level of plasma IL-33. The IL-33 levels were compared among different ARCO stages, CJFH types, and etiology groups. Plasma IL-33 levels were significantly higher in the ONFH patients than that in the control subjects. The levels of IL-33 did not differ significantly among the ONFH patients with different ARCO stages. The IL-33 levels of patients with CJFH type L3 were significantly higher than that of patients with types L1 and L2. No significant differences were observed in IL-33 levels between steroid-induced, alcohol-induced, and idiopathic patients. Our findings seem to indicate that IL-33 effects may be detrimental during ONFH, which appeared to be associated with the prognosis of ONFH. The IL-33 deserves particular attention in the pathogenesis of ONFH.
Objective This study aimed to analyze the changes in serum inflammatory cytokines and anti-inflammatory cytokines in patients with gouty arthritis (GA). Methods The clinical data and serum samples in patients with gouty arthritis and those in healthy volunteers were collected in China-Japan Friendship Hospital from July 2018 to January 2019. Serum cytokine concentrations in patients with GA and volunteers (controls) were determined by a chemiluminescence method. The differences in cytokine concentrations were compared between the two groups. Results Concentrations of serum interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), IL-6, IL-8, and IL-4 were significantly higher in patients with acute GA than in controls. Serum concentrations of IL-1ß, TNF-α, IL-6, IL-8, and immunoglobulin E in patients with remission of GA were significantly lower, whereas concentrations of IL-10 and interferon-γ were significantly higher, compared with those in patients with acute GA. Conclusion This study shows that serum concentrations of IL-1ß, TNF-α, IL-6, IL-8, and IL-4 are significantly elevated in patients with GA, and may be involved in the pathogenesis of GA.
Background Inflammatory bowel disease (IBD) is a functional disorder with chronic and relapsing clinical features. Vasopressin (VP) is a hormone responsible for water and stress homeostasis and also regulates gastrointestinal inflammation and motility. We explored whether VP was related to IBD pathogenesis and its possible pathway. Methods Colitis was induced by 2,4,6‐trinitrobenzenesulfonic acid (TNBS) in mice. The disease activity and colonic damage were evaluated through a scoring system. Locations of the V1a receptor were revealed by immunochemistry method in colon. Ussing chamber technique was performed for the electrophysiological characterization by using rat ileum. The (Arg8)‐Vasopressin (AVP)‐evoked short‐circuit current (Isc) was recorded in the presence of conivaptan (V1a and V2 receptor antagonist), tolvaptan (V1b receptor antagonist), tetrodotoxin (TTX), atropine, cyclooxygenase (COX) inhibitors (indomethacin, nonspecific COX antagonist; SC560, COX‐1 antagonist; NS560, COX‐2 antagonist), and a stabilizer of mast cell (cromolyn sodium), respectively. Key Results TNBS resulted in the obvious loss of body weight and tissue damages in mice. AVP significantly aggravated the TNBS‐induced colitis, which was attenuated by conivaptan but not tolvaptan. V1a receptors were found immunopositive in neurons among the enteric nervous system. AVP evoked a pulsatile response in Isc. Its amplitude, frequency, and cycle duration were around 8‐15 µA/cm2, 10‐11 mHz, and 1.5 minutes, respectively. Notably, the AVP‐evoked change in Isc was abolished by TTX, atropine, conivaptan, indomethacin, NS560, and cromolyn sodium, respectively. Conclusions and Inferences VP‐V1a receptor played the proinflammatory role in TNBS‐induced colitis by promoting COX‐2‐dependent prostaglandin release from mucosal mast cells, which was mediated by the cholinergic pathway.
The response to temperature and glucose, high salt tolerance and self-regulated drug delivery are simultaneously probable by applying a multifunctional microgel in a rational design by a colloid chemistry method. Such smart microgels were fabricated with thermoresponsive N-isopropylacrylamide, glucose-sensitive (2-phenylboronic esters-1,3-dioxane-5-ethyl)methyl acrylate (PBDEMA) and water-soluble crosslinker poly(ethylene glycol) diacrylate through a precipitation emulsion method. These colloidal nanoparticles exhibited PBDEMA-composition-dependent responsive behavior with changing temperature and ionic strength. Amongst them, the microgel with 20.7 mol% PBDEMA with a narrow size distribution is suitable for diabetes treatment because it can adapt to the surrounding medium of different glucose concentrations over a clinically relevant range (0-2.0 mg mL −1 ), control the release of preloaded insulin and is highly stable under normal physiological conditions. Preliminary experiments suggest these highly stable microgels have the potential to be used for self-regulated therapy and monitoring the response to treatment.
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