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Mast Cell Infiltration (mast + cell_infiltration)
Selected AbstractsEffect of mesalazine on mucosal immune biomarkers in irritable bowel syndrome: a randomized controlled proof-of-concept studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2009R. CORINALDESI Summary Background, Intestinal immune infiltration contributes to symptoms in patients with irritable bowel syndrome (IBS). Aim, To assesses the effect of mesalazine (mesalamine) on mucosal immune cells in patients with IBS, through a pilot study. Methods, A randomized, double-blind, placebo-controlled trial in 20 patients with IBS in tertiary care setting. Patients were randomized to receive placebo or 800 mg mesalazine three times daily for 8 weeks. The primary endpoint was a significant reduction in total colonic immune cells on biopsies obtained at the end of treatment compared to baseline. Secondary endpoints included effects on subsets of immune cells, inflammatory mediators and symptom severity. Intention-to-treat analysis was performed. Results, Mesalazine markedly reduced immune cells as compared with placebo (P = 0.0082); this effect was ascribed to a marked inhibition of mast cells (P = 0.0014). Mesalazine significantly increased general well-being (P = 0.038), but had no significant effects on abdominal pain (P = 0.084), bloating (P = 0.177) or bowel habits. No serious drug-related adverse events were reported during the study. Conclusions, Mesalazine is an effective and safe approach to reduce mast cell infiltration and may improve general well-being in patients with IBS. These results support the hypothesis that immune mechanisms represent potential therapeutic targets in IBS. [source] Expression and release of IL-29 by mast cells and modulation of mast cell behavior by IL-29ALLERGY, Issue 10 2010S. He To cite this article: He S, Zhang H, Chen H, Yang H, Huang T, Chen Y, Lin J, Wang F, Chen X, Li T-L, Yang P. Expression and release of IL-29 by mast cells and modulation of mast cell behavior by IL-29. Allergy 2010; 65: 1234,1241. Abstract Background:, The role of interleukin (IL)-29 in innate immunity has been recognized recently, and it is regarded as a potent bioactive molecule. However, little is known about its role in the pathogenesis of allergy. Because mast cells are recognized as primary effector cells of allergy, we investigated the potential relationship between IL-29 and mast cells in this study. Objective:, To examine the expression of IL-29 in mast cells and the influence of IL-29 on mast cell mediator release and accumulation. Methods:, Expression of IL-29 in mast cells was determined by double-labeling immunohistochemistry and flow cytometry analysis. Mast cell cell-line was cultured to examine the mediator release, and mouse peritoneal model was employed to observe the mast cell accumulation. Results:, Large proportions of mast cells expressing IL-29 were localized in human tissue including the colon, tonsil and lung. Mast cells can release substantial quantity of IL-29 upon challenge with proteolytic allergens. Extrinsic IL-29 provoked IL-4 and IL-13 release from mast cell line P815 cells through PI3K/Akt and (JAK)/STAT3 signaling pathways, but failed to induce mast cell histamine release from human mast cells. Extrinsic IL-29 also induced mast cell infiltration in mouse peritoneum by a CD18- and ICAM1-dependent mechanism. Conclusion:, Mast cell-derived IL-29 has the potential to be involved in the pathogenesis of allergic inflammation. [source] Efficacy of pollen immunotherapy in seasonal allergic rhinitisPEDIATRICS INTERNATIONAL, Issue 1 2007DEMET CAN Abstract Background: The efficacy of subcutaneous pollen immunotherapy has been documented in published double-blind, placebo-controlled studies related to treatment of seasonal allergic rhinitis. In the present study, subjective (symptom scores) and objective (nasal peak inspiratory flow, nasal smear, nasal biopsy) parameters were used to study the efficacy of pollen immunotherapy. Methods: Forty-eight patients (32 male), mean ± SE age 13.6 ± 2.8 years allergic to grass-pollen participated in the present study. Patients were divided into three groups: group I, 24 patients who did not receive pollen immunotherapy; group II, 12 patients who received the build-up phase of pollen immunotherapy; and group III, 12 patients who had just finished pollen immunotherapy. With regard to objective and subjective parameters these three groups were compared. Results: When group I was compared to groups II and III, the patients who had not received any immunotherapy were found to have a high daytime nasal symptoms score (P < 0.01), high daytime eye symptoms score(P < 0.01) and high night-time symptoms score (P < 0.01). In objective parameters, it was found that group I had low nasal peak inspiratory flow (P < 0.05), and a high eosinophil count in nasal smears (P < 0.05) and peripheral blood (P < 0.05). It was also demonstrated that there was an increased eosinophil infiltration (P < 0.01) and mast cell infiltration (P < 0.05) in nasal biopsy in group I. There was no significant difference between group II and group III according to these results (P > 0.05). Conclusions: Immunotherapy leads to a better clinical and histopathological prognosis in children with seasonal allergic rhinitis. [source] Expression of eotaxin, interleukin 13 and tumour necrosisfactor-, in dermatitis herpetiformisBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2000P. Amerio Background,The dermal and perivascular infiltrate in dermatitis herpetiformis (DH), which is mainly composed of CD4+ lymphocytes, neutrophils and eosinophils, is believed to play an important part in the pathogenesis of the disease. Previous studies suggest that cytokines such as interleukin (IL) -8, granulocyte-macrophage colony-stimulating factor, IL-4 and IL-5 could be involved in the pathogenesis of DH. These cytokines appear to drive tissue infiltration and maturation of eosinophils. Part of the effect of T-helper (Th) 2-type cytokines (IL-4, IL-5) on eosinophils could be mediated by eotaxin, which is a highly specific chemotactic protein induced by various cytokines [IL-4, IL-13, tumour necrosis factor (TNF) -, and interferon-,]. Objectives,To evaluate the expression of eotaxin and its inducers, IL-13 and TNF-,, in DH. Methods,We examined lesions collected from 10 DH patients with active disease. Sections from each specimen were incubated with anti-IL-13, anti-TNF-, and anti-eotaxin antibodies. Chloroacetyl esterase reaction was performed to show mast cell infiltration. Results,Eotaxin was mainly expressed at the tips of the dermal papillae, within the microabscesses. Positivity was also found in the lymphomonocytic infiltrate in the dermis. IL-13 was expressed in the dermal infiltrate and TNF-, was found in the inflammatory infiltrate and in dermal vascular cells. Conclusions,These findings confirm the importance of the lymphomonocytic infiltrate and of Th2 cytokines in the pathogenesis of this disease, suggesting that tissue infiltration in DH is mediated by cell-specific chemokines such as eotaxin and not only by non-specific chemokines such as IL-8. [source] | ||||||||||