Endoscopic optic nerve decompression for patients with traumatic optic neuropathy: is nerve sheath incision necessary?

OBJECTIVE: To evaluate the necessity of nerve sheath incision for the treatment of patients with traumatic optic neuropathy (TON) during endoscopic optic nerve decompression. METHODS: Seventy-four TON patients were enrolled and subjected to endoscopic optic nerve decompression. In 31 TON patients (group A), osseous decompression and nerve sheath incision were performed, and in 43 TON patients (group B), osseous decompression alone was carried out. Visual acuity was evaluated postoperatively. RESULTS: After surgery, visual acuity was improved in 47 of 74 patients, with a total effectiveness ratio of 63.5%. The total ratio of improvement in groups A and B was 61.2 and 65.1%, respectively, and no significant difference was observed (p > 0.05). As to the patients with residual vision preoperatively, the ratio of improvement in groups A and B was 64.2 and 71.4%, respectively (p > 0.05), not favoring nerve sheath incision during endoscopic optic nerve decompression. CONCLUSION: Our preliminary results suggest that during endoscopic optic nerve decompression for the treatment of TON patients, nerve sheath incision is not obligatory for the improvement of visual acuity.

The antimicrobial protein short palate, lung, and nasal epithelium clone 1 (SPLUNC1) is differentially modulated in eosinophilic and noneosinophilic chronic rhinosinusitis with nasal polyps.

BACKGROUND: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a highly heterogeneous disease with aberrant host defense responses. However, whether innate immunity is similarly impaired in patients with eosinophilic and those with noneosinophilic CRSwNP remains unclear. OBJECTIVES: We sought to evaluate the expression and possible modulation of short palate, lung, and nasal epithelium clone 1 (SPLUNC1), an innate immune molecule, in the 2 CRSwNP subsets. METHODS: Polyp tissue and uncinate processes were collected from 40 patients with CRSwNP, 27 patients with chronic rhinosinusitis without nasal polyps (CRSsNP), and 22 control subjects. Expression of SPLUNC1; Toll-like receptor (TLR) 2, TLR3, and TLR4; and the proinflammatory cytokines IL-1α, IL-4, IL-13, IL-17A, and IFN-γ was examined in nasal tissues. Additionally, SPLUNC1 expression in response to specific inflammatory stimulation was measured in cultured polyp epithelial cells and A549 cells. RESULTS: Polyp tissues exhibited significantly decreased expression of SPLUNC1 and other innate immune molecules compared with uncinate process tissues from patients with CRSwNP (P < .05), patients with CRSsNP, and healthy control subjects. Moreover, the eosinophilic CRSwNP subset exhibited significantly decreased SPLUNC1 expression and numbers of submucosal glands, as well as significantly increased IL-4 and IL-13 mRNA levels, compared with the noneosinophilic subset (P < .05). Accordingly, SPLUNC1 expression in polyp epithelial cells was significantly inhibited by IL-4 and IL-13 stimulation in vitro but was significantly upregulated after stimulation with TLR agonists and glucocorticoids (P < .05). CONCLUSION: Differential SPLUNC1 suppression between the eosinophilic and noneosinophilic CRSwNP subsets suggests that they possess distinct pathogenic mechanisms. This finding might benefit the design of appropriate therapeutic interventions targeted to each subset.

Suppression of connexin 26 is related to protease-activated receptor 2-mediated pathway in patients with allergic rhinitis.

BACKGROUND: Connexin (Cx) 26 plays a key role in maintaining the integrity of tight junctions. However, the expression and modulation of Cx26 in allergic rhinitis (AR) has not been well understood. METHODS: We detected the expression of Cx26 in house-dust mite (HDM)-sensitized AR patients and investigated the Cx26 production and modulation in primary human nasal epithelial cells (HNECs) and BEAS-2B cells after treatment with the allergen Der p 1 from Dermatophagoides pteronyssinus. RESULTS: We found that the mRNA and protein levels of Cx26 were significantly down-regulated in AR patients compared with the control. Der p 1 was found to induce protease-activated receptor 2 (PAR2) expression and suppress Cx26 production significantly in vitro. PAR2 siRNA was shown to prevent the suppression of Cx26 induced by Der p 1 in BEAS-2B cells. CONCLUSION: The suppression of Cx26 in HDM-sensitized AR patients is related to a PAR2-mediated pathway and might serve during the initiation and maintenance of AR. Targeting the PAR2-mediated Cx26 suppression may be a potential means of preventing allergic sensitization.