Measurement of Inflammatory Mediators of Mast Cells and Eosinophils in Native Nasal Lavage Fluid in Nasal Polyposis

Abstract

Background: Nasal polyposis (NP) often coexists with asthma, rhinitis and sinusitis. Polyp histology typically shows chronic, eosinophilic inflammation. The inflammatory cell infiltrate generally includes eosinophils, lymphocytes, plasma cells and mast cells. Objective: To gain insight into the natural history of NP, we analysed mediator levels and leukocyte values in nasal fluids and eosinophil cationic protein (ECP), total IgE levels and eosinophils in the blood in several groups of both allergic and non-allergic patients with nasal polyps and in patients with allergic rhinitis (AR). Methods: Thirty-two patients with nasal polyps entered the study. As a control group, we studied 55 patients with AR, i.e. 20 patients with seasonal AR to grass pollen, 24 with AR sensitive to Parietaria and 11 with AR sensitive to house dust mite (HDM). Eighteen patients with nasal polyps were also allergic patients (8 were sensitive to Parietaria and 10 were sensitive to HDM), whereas 14 were non-allergic patients. Tryptase and histamine values were assayed in nasal fluids, whereas total IgE was determined in serum. ECP values were assayed both in nasal fluids and serum. Eosinophils were quantified both in the blood and nasal fluids. Results: Tryptase levels were significantly higher in the nasal lavages from patients with NP than in those from patients without NP (4.7 vs. 3.5 U/l, p < 0.001) and correlated with symptom scores (r_s = 0.42, p < 0.0001). The median levels of histamine in nasal fluids from patients with NP were also significantly higher than those observed in patients without NP (50.0 vs. 21.3 ng/ml, p < 0.001), but did not correlate with symptom scores. Finally, the median levels of ECP in nasal fluids from patients with NP were significantly higher than those observed in patients without NP (38.1 vs. 16.1 ng/ml, p < 0.001) and correlated with symptom scores (r_s = 0.38, p < 0.001). Analysis of variance showed that, among the variables studied, the presence of nasal polyps was the factor responsible for the higher levels of tryptase, histamine and ECP in nasal fluids. With regard to leukocyte counts in nasal fluids, no significant differences were observed between rhinitis patients with NP and those without NP. With regard to serum ECP and serum total IgE, no significant differences were detected between the two groups under study. Blood eosinophil levels in patients with NP were significantly higher than those observed in patients without NP (5.8 vs. 5.6, p = 0.002). Analysis of variance showed that both the presence of nasal polyps and the type of sensitisation were important. Considering the total symptom scores, no significant differences were observed between rhinitis patients with NP and those without NP. Conclusions: The present findings are consistent with the view that chronic eosinophil mucosal inflammatory disease in NP involves a self-sustaining mechanism, i.e. local release of inflammatory mediators, independent of allergen stimulation of nasal mucosa. Increased release of inflammat...

Increased IL-6 and IL-4 in exhaled breath condensate of patients with nasal polyposis

“…We also demonstrated a positive correlation between nasally exhaled IL-6 with number of neutrophils in nasal scraping and nasally exhaled IL-4 with number of eosinophils in nasal scraping. Nasal polyposis is characterised by infiltration of inflammatory cells, including mast cells, eosinophils, lymphocytes and neutrophils [19]. Although the exact mechanism elucidating the pathogenesis of NP is not clearly understood, a wide spectrum of cytokines seems to play an important role in developing NP [20].…”

“…The pro-inflammatory cytokines IL-4, which modulates the function of eosinophils and is widely produced by T cells and mast cells, and IL-6, which actively participate to the inflammatory response, and is mainly released by neutrophils and macrophages [21], permanently contribute to perpetuate the mucosal inflammation of patients with NP. IL-4 has been previously utilised to investigate eosinophilic inflammation in nasal lavage of patients with NP [19], is also able to induce cells apoptosis and to promote airway eosinophilia [22]. IL-6 has been widely studied in inflammatory diseases and has been previously found enhanced in nasal polyps epithelial cell-conditioned medium and in polyps tissue of subjects with NP [23].…”

Apafant, a Potent Platelet-Activating Factor Antagonist, Blocks Eosinophil Activation and Is Effective in the Chronic Phase of Experimental Allergic Conjunctivitis in Guinea Pigs

“…In the present work, we have investigated whether or not PAF activates eosinophils in the conjunctival tissues by measuring EPO activities, as an eosinophil activation marker (3,4), in the OLF after the application of PAF into the conjunctival sac of guinea pigs. EPO is one of the specific eosinophil granule proteins, which are detected in the tear fluid of patients with allergic conjunctivitis, and their levels have been correlated with the severity of the disease (18).…”

“…The eosinophil granule proteins, such as major basic protein, eosinophil cationic protein, eosinophil neurotoxin, and eosinophil peroxidase (EPO), are released by activated eosinophils and their cytotoxic activity may play an important role in the chronicity and exacerbation of allergic conjunctivitis. The presence of these proteins in biological fluids is now considered a specific marker for eosinophil activation (3,4) and is used as a clinical diagnosis to monitor the severity of allergic diseases.…”

Polipose nasal: caracterização da infiltração dos eosinófilos, mastócitos, miofibroblastos e células TGF-beta positivas em indivíduos com e sem asma

“…Na PN os mastócitos pela micro localização na profundeza do estroma ( Pawliczak et al 1997, Finotto et al 1994, Kawabori et al 1992, Drake-Lee e Price 1997, Sasaki 1986) vão de forma direta, induzir a inflamação eosinofílica através da liberação de vários mediadores inflamatórios (Pawankar 2003, Di Lorenzo et al 2001, ou indiretamente, através da ativação de células estruturais (fibroblastos e miofibroblastos) contribuindo para a formação e progressão dos pólipos nasais.…”