Ewing's sarcoma/primitive neuroectodermal tumour occurring in the maxillary sinus.

A 12-year-old boy complained of swelling of the left cheek. Fiberscopic examination revealed the presence of a soft reddish mass in the middle meatus of the left nostril. CT scan showed a large mass completely filling the left maxillary sinus. The lesion originated from the maxillary sinus and extended to the middle nasal meatus; bone destruction and invasion of the subcutaneous tissue of the cheek were noted. T2-weighted MRI images revealed a heterogeneous signal in the left maxillary sinus. Under general anaesthesia, biopsies were obtained through an intraoral incision. On pathology, atypical cells containing irregular nuclei with scanty cytoplasm were noted. The tumour cells were strongly positive for CD99 and reacted weakly with NSE however the cells were negative for synaptophysin, LCA and cytokeratin on immunohistochemical examination. Based on these findings, the tumour was diagnosed as a Ewing's sarcoma/primitive neuroectodermal tumour. The patient was treated with radiotherapy and combination chemotherapy; subsequently, the tumour's size decreased markedly. After 20 months of follow-up, the patient showed no evidence of local tumour growth or metastasis.

IL-4 and TNF-alpha increased the secretion of eotaxin from cultured fibroblasts of nasal polyps with eosinophil infiltration.

BACKGROUND: Nasal polyposis is considered a subgroup of chronic rhinosinusitis (CRS). Eosinophils are the most common inflammatory cells in nasal polyp and the degree of the tissue eosinophilia is correlated with the probability of the recurrence of nasal polyps. However, the mechanism by which eosinophils are selectively recruited in nasal polyp remains to be clarified. In the present study, fibroblasts were isolated from nasal polyps of patients with eosinophil-rich nasal polyps (Enp) and those with non-eosinophilic nasal polyps (NEnp) and the secreted levels of eotaxin, regulated upon activation normal T expressed and presumably secreted (RANTES), and vascular cell adhesion molecule-1 (VCAM-1) from the cultured fibroblasts were determined. The levels were compared between Enp and Nenp. The role of those chemokines and adhesion molecules in the pathogenesis of nasal polyp is discussed. METHODS: Fibroblasts isolated from nasal polyps of five patients with CRS with Enp and four patients with CRS with NEnp were cultured and stimulated with 10 ng/ml of tumor necrosis factor-alpha (TNF-alpha) and interleukin-4 (IL-4) for 24 hours. After stimulation, culture supernatants were collected and concentrations of eotaxin, RANTES, and VCAM-1 were quantified by Enzyme linked immunosorbent assay (ELISA). RESULTS: TNF-alpha enhanced the secretion of VCAM-1 and RANTES by fibroblasts derived from both NEnp and Enp, but did not affect the release of eotaxin. IL-4 increased the secretion of VCAM-1 and eotaxin but not that of RANTES. Furthermore, TNF-alpha and IL-4, when added together, induced a synergistic effect on the secretion of VCAM-1 and eotaxin. The effect of IL-4 and IL-4 plus TNF-alpha on eotaxin release was more marked for Enp fibroblasts compared with NEnp fibroblasts. CONCLUSIONS: The results suggest that eotaxin plays an important role in the selective recruitment of eosinophils in Enp. Nasal fibroblasts in Enp are more sensitive than those in NEnp regarding eotaxin release induced by the stimulation with IL-4 and co-stimulation with TNF-alpha and IL-4. This difference might be associated with the pathogenesis of nasal polyposis having marked accumulation of eosinophils.

Intranasal immunization with phosphorylcholine induces antigen specific mucosal and systemic immune responses in mice.

Phosphorylcholine (PC) is a structural component of a wide variety of pathogens including Streptococcus pneumoniae and Haemophilus influenzae, and anti-PC immune responses are known to protect mice against invasive bacterial diseases. The present study tested the capability of PC as an intranasal plurispecific vaccine against upper airway infections. BALB/c mice immunized with intranasal PC-keyhole limpet hemocyanin (KLH) plus cholera toxin (CT) as a mucosal adjuvant showed increased PC-specific IgM in serum, IgA in nasal wash and saliva, and numbers of PC-specific nasal and splenic antibody producing cells. Enhanced production of IL-4 and IFN-gamma by CD4+ T cells indicated the participation of Th2- and Th1-type cells. Salivary IgA antibodies produced by intranasal immunization with PC-KLH plus CT reacted to most strains of S. pneumoniae and H. influenzae. Further we demonstrated that the clearance of S. pneumoniae and H. influenzae from the nasal tract was significantly enhanced by nasal immunization with PC-KLH and CT. Thus, intranasal vaccination to induce PC-specific immune responses might help to prevent upper airway infections caused by S. pneumoniae and H. influenzae.

TNF-alpha upregulates VCAM-1 and NF-kappaB in fibroblasts from nasal polyps.

OBJECTIVE: Lung and synovial fibroblasts produce VCAM-1 in response to TNF-alpha. However, the massive infiltration of eosinophils, the effects of the increased amount of TNF-alpha and the production of VCAM-1 in human nasal polyp fibroblasts are not yet fully understood. The present study examines the role of VCAM-1 and the molecular mechanism of its expression in nasal fibroblasts. METHODS: Nasal fibroblasts were isolated from human nasal polyps and after four passages, the cells were stimulated with TNF-alpha and VCAM-1 expression was examined by ELISA, flow cytometry, and RT-PCR. The activation of NF-kappaB induced by TNF-alpha was determined by electrophoretic mobility shift assays and the influence on the expression of VCAM-1 was investigated. RESULTS: VCAM-1 protein and mRNA were expressed in unstimulated controls and remarkably increased by TNF-alpha stimulation. NF-kappaB activity was enhanced by TNF-alpha stimulation and remarkably suppressed by NF-kappaB proteasome inhibitor. CONCLUSIONS: The present study discovered that nasal fibroblasts produce VCAM-1 protein and mRNA and that production is increased by TNF-alpha stimulation. Furthermore, VCAM-1 expression in nasal fibroblasts is induced through an NF-kappaB-dependent pathway. These findings might provide a rationale for using NF-kappaB inhibitors as a treatment for nasal inflammatory diseases such as polyps.