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There are many humoral factors that regulate the migration of mast cell progenitors from the blood into tissues and the migration of mature mast cells within tissues, leading to the rapid accumulation that occurs in diverse pathological conditions. First of all, mast cell migration is stimulated by some chemokines, such as RANTES, eotaxin, and IL-8. Moreover, many cytokines induce the migration of mast cells (i.e. SCF, TNF, IL-15). Finally, the migration of mast cells is also stimulated by many other humoral factors, including those involved in inflammatory process, such as C3a, C5a, histamine, PAF, and CRP. Because mast cells play an essential role in diverse physiological and pathological processes, it seems to be of great importance to know the mechanisms underlying the migration of immature and mature mast cells. However, current knowledge about these processes is still insufficient.

Introduction: According to the results of research carried out by a number of authors, one of the main mechanisms of the generation of polyps is local inflammatory processes accompanied by immune system disorders. It has recently been shown that a number of differentiation factors and inflammatory mediators may be involved in the growth of nasal polyps. RANTES is a eosinophil chemoattractant factor likely could play an important role in a chronic inflammatory response in the nasal tissue that subsequently leads to the development of nasal polyps., Objective: The objective of this study was detection of the chemokine RANTES in nasal polyps fibroblasts and researching influence of stimulation with lipopolisaccharides and phytohemagglutinin for RANTES expression in cultured nasal fibroblasts in vitro., Methods: Nasal polyps were obtained from 17 subjects (9 atopic and 8 nonatopic) during polypectomy. RANTES was measured by immunofluorescence method., Results: Intensive granular luminescence was observed in all cytoplasm of cells with the exception of nucleus. Immunoreactive RANTES was found to be present in 70% of cells. We not find increase percentage of positive RANTES fibroblasts after stimulation with lipopolisaccharides and phytohemagglutinin. RANTES expression was similar in the both: atopic and nonatopic polyps., Conclusions: This study demonstrates that cultured fibroblasts derived from both atopic and nonatopic patients release RANTES spontaneously and after stimulation with lipopolisaccharides and phytohemagglutinin. This observation and the finding that RANTES is present in nasal polyps fibroblasts suggest that this chemokine may be an important mediator of eosinophil in both atopic and nonatopic nasal polyposis. More research needs to expand on chemotactic factors such as RANTES and their interplay with other local cytokines.

Background: [corrected] Allergic rhinitis is one of risk factors for development of allergic asthma., Methods: 9 patients with asthma, 16 patients with seasonal allergic rhinitis (SAR) due to grass or rye pollen sensitization and 17 healthy control subjects were recruited to the study. SAR patients were identified by history, skinprick test, specific IgE and positive nasal allergen challenge. Every subject underwent the methacholine bronchial provocation test and sputum induction. Levels of RANTES were measured in supernatant of induced sputum., Results: Increased percentage of eosinophils in induced sputum in asthma compared to control group (p=0.01) but not in SAR patients compared to healthy subjects (p=0.13) were found. Similarly, asthmatic patients (p=0.01) but not SAR patients had increased levels of RANTES in sputum compared to healthy subjects., Conclusion: Increased levels of RANTES in induced sputum of patients with chronic asthma but not in SAR patients indicate that RANTES is important in pathogenesis of chronic airway inflammation.

Eosinophils are important cells of inflammatory infiltration in respiratory tract of asthmatics patients. Rantes is a potent chemotactic agent for eosinophils. It belongs to the chemokine family. Heparin has been reported to diminish size of allergen skin tests and decrease response to allergen bronchoprovocation in allergic asthma. We have found that heparin diminished late phase of allergic reaction and inhibits allergen induced increase in specific and nonspecific bronchial hyperresponsiveness. In order to explore the mechanism involved in these protective effects we studied the influence of heparin on eosinophil chemotaxis induced by Rantes and FMLP. Eosinophils were isolated from peripheral blood of 12 asthmatic donors. Chemotaxis was evaluated using polycarbonate filters in 48-well chemotactic chamber. The table shows the results (*) p < 0.05. [table: see text] Ten minutes exposure of eosinophils to heparin was sufficient for inhibition. Removal to heparin by washing the cells ablated observed effects. Preincubation of Rantes or FMLP with heparin did not induce any significant changes in eosinophil chemotaxis. Heparin alone did not posess any chemotactic activity for eosinophils. Our results suggest that heparin ameliorate allergic inflammation by inhibition of eosinophil flux and this inhibition is a surface phenomenon.