IL-32 is a described pro-inflammatory cytokine produced by T lymphocytes, natural killer cells, monocytes, and epithelial cells. However, the specific mechanism of IL-32 on allergic rhinitis (AR) has not been elucidated. Here, we report a significant increase of IL-32 protein and mRNA in the nasal mucosa of AR patients. In addition, in nasal mucosa tissue from AR patients, the level of IL-32 production correlated with inflammation, IL-1β, IL-18, and granulocyte-macrophage colony-stimulating factor (GM-CSF). In an AR animal model, IL-32 significantly increased IgE and inflammatory cytokine levels. IL-32 expression was induced by recombinant human GM-CSF via activation of caspase-1 in eosinophils. In addition, depletion of IL-32 prevents the production of inflammatory cytokines in eosinophils. In conclusion, IL-32 is an important cytokine involved in the inflammation of AR. The regulation of IL-32 expression may form the basis of a new strategy for the treatment of AR.

IntroductionInterleukin (IL)-32 is an inflammatory cytokine induced by Mycobacterium tuberculosis and Mycobacterium bovis in a variety of cell types and discovered in the synovial of patients with rheumatoid arthritis (RA). Thymic stromal lymphopoietin (TSLP) play several roles in the pathogenesis of RA. However, the role of IL-32 and TSLP in RA has not been elucidated.MethodsWe evaluated the specific mechanism of between IL-32 and TSLP in RA using human monocyte cell line, THP-1 cells.ResultsHere we documented for the first time that IL-32 highly increased TSLP production in THP-1 cells and human blood monocytes. TSLP expression was induced by IL-32 via activation of caspase-1 and nuclear factor-κB. TSLP produced by IL-32 increased differentiation of monocytes but depletion of TSLP prevented differentiation of monocytes into macrophage-like cells. Chondroprotective drugs such as chondroitin sulfate (CS) and the traditional Korean medicine, BaekJeol-Tang (BT) decrease production of TSLP and activation of caspase-1 and nuclear factor-κB. In addition, CS and BT inhibited IL-32-induced monocytes differentiation.ConclusionsTaken together, IL-32 and TSLP are important cytokines involved in the development of RA. The effects of CS and BT were associated with the downregulation of TSLP and caspase-1 through negative regulation of IL-32 pathways in RA.

BackgroundBacterial meningitis is an infectious disease with high rates of mortality and high frequency of severe sequelae. Early identification of causative bacterial and viral pathogens is important for prompt and proper treatment of meningitis and for prevention of life-threatening clinical outcomes. In the present study, we evaluated the value of the Seeplex Meningitis ACE Detection kit (Seegene Inc., Korea), a newly developed multiplex PCR kit employing dual priming oligonucleotide methods, for diagnosing acute meningitis.MethodsAnalytical sensitivity of the kit was studied using reference strains for each pathogen targeted by the kit, while it's analytical specificity was studied using the human genome DNA and 58 clinically well-identified reference strains. For clinical validation experiment, we used 27 control cerebrospinal fluid (CSF) samples and 78 clinical CSF samples collected from patients at the time of diagnosis of acute meningitis.ResultsThe lower detection limits ranged from 101 copies/µL to 5×101 copies/µL for the 12 viral and bacterial pathogens targeted. No cross-reaction was observed. In the validation study, high detection rate of 56.4% was obtained. None of the control samples tested positive, i.e., false-positive results were absent.ConclusionsThe Seeplex Meningitis ACE Detection kit showed high sensitivity, specificity, and detection rate for the identification of pathogens in clinical CSF samples. This kit may be useful for rapid identification of important acute meningitis-causing pathogens.

A Gram-positive, rod-shaped bacterium, designated strain LBY T , was isolated from the blood of a Korean patient. The organism could not be identified based on conventional clinical microbiological methods. 16S rRNA gene sequencing and phylogenetic analysis revealed that it belonged to the genus Paenibacillus, but was distinct from recognized Paenibacillus species. Strain LBY T was related most closely to the type strains of Paenibacillus macerans and Paenibacillus popilliae, with 16S rRNA gene sequence similarities of 96.2 and 95.4 %, respectively. The major fatty acids of strain LBY T were anteiso-C 15 : 0 (43.8 %), C 16 : 0 (10.4 %), iso-C 16 : 0 (10.3 %), iso-C 15 : 0 (9.2 %) and anteiso-C 17 : 0 (8.3 %). On the basis of biochemical characteristics, fatty acid composition and comparative 16S rRNA gene sequence analysis, strain LBY T is considered to represent a novel species of the genus Paenibacillus, for which the name Paenibacillus konsidensis sp. nov. is proposed. The type strain is LBY T (5ABB-ID-KSY9 T 5KCTC 13165 T 5JCM 14798 T ).The genus Paenibacillus, which was defined by Ash et al. (1993) on the basis of 16S rRNA gene sequence analysis, comprises facultatively anaerobic or strictly aerobic, rodshaped bacteria with DNA G+C contents ranging from 45 to 54 mol%. Members of the genus Paenibacillus have been isolated from a variety of sources, including soil, the rhizosphere, water, diseased insect larvae and foods, and they show physiologically diverse characteristics (Daane et al., 2002). A few Paenibacillus species are pathogenic. For example, Paenibacillus alvei, Paenibacillus macerans and Paenibacillus polymyxa have been isolated from patients suffering from meningitis, sickle cell anaemia, wound infection and ovine abortion (Logan & Turnbull, 2003).Here we describe the isolation of a Paenibacillus-like bacterial strain, designated LBY T , from a febrile patient. Results of 16S rRNA gene sequencing and biochemical testing indicate that this bacterial isolate represents a novel species of the genus Paenibacillus.A 75-year-old male who had been in a long-term care facility was transferred to our emergency room due to a fever that had persisted for 2 weeks. Upon admission, he developed haematemesis and hypotension. Two sets of blood were drawn for the cultures, and they were found to harbour Gram-positive rod-shaped bacteria. However, these isolates could not be identified by using conventional methods in the clinical microbiology laboratory, including VITEK (bioMérieux) and Microscan (Dade-Microscan) analyses. To isolate the bacterium, blood samples were inoculated into standard BacT/Alert bottles (bioMérieux) and incubated at 37 u C. Bottles showing a positive signal were sampled aseptically and inoculated onto blood agar plates. The plates were incubated at 37 u C in air with 5 % CO 2 .Abbreviation: CFA, cellular fatty acid.3These authors contributed equally to this study.The GenBank/EMBL/DDBJ accession number for the 16S rRNA gene sequence of strain LBY T is EU081509. Colonies of strain LBY T were...

The objectives of this study were to explore whether ovarian vascular endothelial growth factor (VEGF) expression in mice can be regulated by IL-6 (interleukin-6), angiotensin II, FSH, and hCG; and to test whether the mouse ovarian VEGF expression can result in angiogenesis. The ICR mice were sacrificed, and their ovaries were recovered. Recovered ovaries were treated with IL-6, angiotensin II, FSH, and hCG separately and incubated for 24 hours in α-MEM. Expression of mRNA and protein of VEGF were assessed by RT-PCR and immunohistochemistry. The resulting angiogenesis was evaluated through immunohistochemical analysis for CD34. Treatment of mice ovaries with IL-6, FSH, and hCG resulted in a significant increase of VEGF mRNA, and IL-6 was the most potent inducer of VEGF. IL-6 and FSH resulted in increased neovascularization in the follicular phase of mouse ovaries. In contrast, angiotensin II could not increase VEGF expression or neovascularization. We documented an in vitro increase in VEGF expression by IL-6, FSH, and hCG; and reaffirmed that the proliferative response of murine ovarian endothelial cells paralleled an increase of VEGF expression.