Inhibited experimental corneal neovascularization by neutralizing anti-SDF-1α antibody

AIM: To explore the effect of SDF-1α on the development of experimental corneal neovascularization (CRNV). METHODS: CRNV was induced by alkali injury in mice. The expression of SDF-1α and CXCR4 in burned corneas was examined by Flow Cytometry. Neutralizing anti-mouse SDF-1α antibody was locally administrated after alkali injury and the formation of CRNV 2 weeks after injury was assessed by Immunohistochemistry. The expression of VEGF and C-Kit in burned corneas was detected by RT-PCR. RESULTS: The number of CRNV peaks at 2 weeks after alkali injury. Compared to control group, SDF-1α neutralizing antibody treatment significantly decreased the number of CRNV. RT-PCR confirmed that SDF-1α neutralizing antibody treatment resulted in decreased intracorneal VEGF and C-Kit expression. CONCLUSION: SDF-1α neutralizing antibody treated mice exhibited impaired experimental CRNV through down regulated VEGF and C-Kit expression.     

Diagnostics of Sjögren's syndrome by means of anti-alpha-fodrin antibody

BACKGROUND: Sj?gren's syndrome (SS) is a common connective tissue disease concerning 0.5 % of the white population. Typical symptoms are dry eyes and a dry mouth. The diagnostics of SS often are difficult, especially during early stages of the disease as long as the leading symptoms have not yet fully developed. Previously employed serum antibodies have neither been sensitive nor specific enough to be able to differentiate SS from different rheumatic diseases. We report on a patient with relapsing corneal erosions. In his case we have been able to support the diagnosis of SS by detecting the anti-alpha-fodrin-antibody as well as antinuclear antibodies. CASE REPORT: The patient appeared with incomplete closure of the eyelids and corneal ulcers on both eyes. Smears of the conjunctivae from both eyes were sterile. Schirmer's test indicated a decrease in tear production with 5 mm in the right eye and a normal tear production with 19 mm in the left eye. Three months before, the results of this test had been even more pronounced with 1 mm and 3 - 4 mm, respectively. Additionally the patient described relapsing erosions and a dry mouth. We then examined his blood to help diagnose SS. Results were negative for rheumatoid factor, anti-Ro/SSA antibody and anti-La/SSB antibody, but positive for anti-nuclear-antibodies. In order to spare the patient an invasive biopsy we examined the anti-alpha-fodrin-antibody which was positive. CONCLUSION: Even with negative anti-Ro/SSA and anti-La/SSB antibodies the positive anti-alpha-fodrin-antibody supported the diagnosis of SS. Therefore, we consider it a useful addition to the diagnostics previously employed in the diagnosis of SS (Schirmer's-test, anti-Ro/SSA-AK, anti-La/SSB-AK, rheumatoid factor, eventually biopsy).     

Subunit-specific polyclonal antibody targeting human ρ1 GABA(C) receptor

The GABA_C receptor, a postsynaptic membrane receptor expressed prominently in the retina, is a ligand-gated ion channel that consists of a combination of ρ subunits. We report characterization of a novel guinea pig polyclonal antibody, termed GABA_C Ab N-14, directed against a 14-mer peptide (N-14) of the extracellular domain of the human ρ1 subunit. The antibody exhibits high sensitivity for N-14 by ELISA. In Western blots, GABA_C Ab N-14 shows reactivity with the ρ1 subunit of preparations obtained from ρ1 GABA_C-expressing neuroblastoma cells, Xenopus oocytes, and mammalian retina and brain. Flow cytometry reveals a rightward shift in mean fluorescence intensity of GABA_C-expressing neuroblastoma cells probed with GABA_C Ab N-14. Immunostaining of neuroblastoma cells and oocytes with GABA_C Ab N-14 yields fluorescence only with GABA_C-expressing cells. Antibody binding has no effect on GABA-elicited membrane current responses. Immunostaining of human retinal sections shows preferential staining within the inner plexiform layer. GABA_C Ab N-14 appears well suited for investigative studies of GABA_C ρ1 subunit in retina and other neural tissues.     

Correlation between elevation of serum antinuclear antibody titer and decreased therapeutic efficacy in the treatment of Beh?et’s disease with infliximab

Background

Infliximab, an anti-TNF-α monoclonal antibody, administered to Beh?et’s disease (BD) patients in Japan with refractory intraocular inflammation, has shown excellent clinical results. However, some patients demonstrate a decreased response to infliximab during the course of the treatment. In the present study, we investigated the correlation between this reduced therapeutic effect and elevation of the serum antinuclear antibody (ANA) titers in patients with BD who were undergoing infliximab therapy.

Methods

Seventeen patients (14 males and three females) with uveitis in BD who were undergoing treatment with infliximab for 2?years or longer were enrolled. Their blood test results and clinical histories were obtained from medical records.

Results

One patient (5.9%) was ANA-positive prior to the initiation of infliximab, and 11 patients (64.7%) developed positive ANA during the therapy. The appearance of ANA was observed 6?months after the initiation of the infliximab therapy, and its titers gradually increased. None of the patients showed lupus symptoms. Five patients (29.4%) have suffered from ocular inflammatory attacks since the sixth month from the initiation of infliximab treatment and all of them were ANA-positive. In contrast, four patients (23.5%) who were ANA-negative experienced no ocular attacks during the follow-up period.

Conclusions

Here we report the positive conversion and subsequent elevation of serum ANA titers in some patients with BD after the initiation of infliximab therapy. Since all recurrences of uveitis were shown only in the ANA-positive patients, serum ANA titer may be a helpful biomarker for predicting the recurrence of ocular attacks in BD patients treated with anti-TNF-α antibody therapies.