Eosinophil Degranulation Patterns in Nasal Polyposis: An Ultrastructural Study

2009 ◽  
Vol 23 (5) ◽  
pp. 466-470 ◽  
Author(s):  
Miguel Armengot ◽  
Luis Garín ◽  
Carmen Carda

Background Eosinophils are possibly the most important inflammatory cells in the pathogenesis of rhinosinusitis with nasal polyposis. Eosinophil degranulation is the mechanism by which these cells exert their inflammatory action. Knowledge of eosinophil state and degranulation mode therefore may help us to better understand this disease. A study is made of eosinophil state and degranulation mode using transmission electron microscopy (TEM), attempting to establish correlations with certain clinical variables considered to be of importance in patients with nasal polyposis. Methods A prospective TEM study was made to examine 582 eosinophils under 5000× magnification, classifying them according to their state and degranulation mode. The cells originated from 36 cases of nasal polyposis and were catalogued according to the clinical–radiological presentation of the disorder, the presence of asthmatic disease, or acetilsalicilic acid (ASA) triad syndrome (nasal polyposis, asthma, and nonsteroidal anti-inflammatory drug intolerance), and the degree of nasal tissue eosinophilia of the case of origin. Results A total of 30.75% of the eosinophils were inactive, 41.75% exhibited piecemeal degranulation (PMD), 27.5% exhibited cytolysis, and 0.34% were in apoptosis. The degranulation mode was significantly correlated to the clinical and histological parameters studied. Thus, cytolysis tended to be less pronounced and PMD greater, in the cells from cases with intense eosinophilia or severe polyposis (high clinical stage and ASA triad). Conclusion Cytolysis and PMD are the principal degranulation modes of eosinophils in nasal polyposis—apoptosis being very infrequent. Nasal polyposis shows a correlation between eosinophil degranulation mode and the clinical and radiological stage and the degree of tissue eosinophilia of the case of origin.

2019 ◽  
Vol 33 (4) ◽  
pp. 395-402 ◽  
Author(s):  
Giuseppe Brescia ◽  
Franco Schiavon ◽  
Lorenzo Nicolè ◽  
Elisabetta Zanoletti ◽  
Claudia Zanotti ◽  
...  

Background An example of aggressive eosinophilic polyposis can be found in eosinophilic granulomatosis with polyangiitis (EGPA). Intercellular adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule-1 (vCAM-1) play a part in mediating the recruitment and adhesion of leukocytes to the vessel wall, and their blood-to-tissue migration under inflammatory conditions. Objective This prospective study compared 3 groups—patients with a definite diagnosis EGPA, non-EGPA patients with phenotypic features suggestive of EGPA, and patients with non-eosinophilic nasal polyposis (controls)—in terms of nasal tissue histology, iCAM-1 and vCAM-1 expression, and blood inflammatory cells. Methods A total of 58 adults underwent sinus surgery (13 patients with EGPA, 23 suspected of having EGPA, and 22 controls). Results Mean tissue eosinophil counts were significantly higher in EGPA patients and suspected cases of EGPA than in controls. Although iCAM-1 and vCAM-1 were diffusely expressed in sinonasal tissues, they did not differently stain EGPA, eosinophilic-type and non-eosinophilic polyposis. Blood basophil and eosinophil levels were high in both the EGPA and the suspected EGPA groups. Intergroup differences were found for eosinophils but not for basophils. Conclusions We do not have yet blood or tissue markers able to differentiate the early phase of EGPA from chronic rhinosinusitis with nasal polyps. Further investigations are mandatory considering EGPA patients at their initial diagnosis and before any treatment, in terms of nasal histology and blood inflammatory cells, to identify markers characterizing sinonasal mucosa inflammation and useful for an early diagnosis of EGPA.


BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Azer Farah ◽  
Maria Kabbage ◽  
Salsabil Atafi ◽  
Amira Jaballah Gabteni ◽  
Mouadh Barbirou ◽  
...  

Abstract Background Gastric and colorectal cancers are the most common malignant tumours, leading to a significant number of cancer-related deaths worldwide. Recently, increasing evidence has demonstrated that cancer cells exhibit a differential expression of potassium channels and this can contribute to cancer progression. However, their expression and localisation at the somatic level remains uncertain. In this study, we have investigated the expression levels of KCNB1 and KCNA5 genes encoding ubiquitous Kv2.1 and Kv1.5 potassium channels in gastric and colorectal tumours. Methods Gastric and colorectal tumoral and peritumoral tissues were collected to evaluate the expression of KCNB1 and KCNA5 mRNA by quantitative PCR. Moreover, the immunohistochemical staining profile of Kv2.1 and Kv1.5 was assessed on 40 Formalin-Fixed and Paraffin-Embedded (FFPE) gastric carcinoma tissues. Differences in gene expression between tumoral and peritumoral tissues were compared statistically with the Mann-Whitney U test. The association between the clinicopathological features of the GC patients and the expression of both Kv proteins was investigated with χ2 and Fisher’s exact tests. Results The mRNA fold expression of KCNB1 and KCNA5 genes showed a lower mean in the tumoral tissues (0.06 ± 0.17, 0.006 ± 0.009) compared to peritumoral tissues (0.08 ± 0.16, 0.16 ± 0.48, respectively) without reaching the significance rate (p = 0.861, p = 0.152, respectively). Interestingly, Kv2.1 and Kv1.5 immunostaining was detectable and characterised by a large distribution in peritumoral and tumoral epithelial cells. More interestingly, inflammatory cells were also stained. Surprisingly, Kv2.1 and Kv1.5 staining was undoubtedly and predominantly detected in the cytoplasm compartment of tumour cells. Indeed, the expression of Kv2.1 in tumour cells revealed a significant association with the early gastric cancer clinical stage (p = 0.026). Conclusion The data highlight, for the first time, the potential role of Kv1.5 and Kv2.1 in gastrointestinal-related cancers and suggests they may be promising prognostic markers for these tumours.


Blood ◽  
1998 ◽  
Vol 92 (3) ◽  
pp. 778-783 ◽  
Author(s):  
Birgit Dibbert ◽  
Isabelle Daigle ◽  
Doris Braun ◽  
Corinna Schranz ◽  
Martina Weber ◽  
...  

Eosinophils are potent inflammatory cells involved in allergic reactions. Inhibition of apoptosis of purified eosinophils by certain cytokines has been previously shown to be an important mechanism causing tissue eosinophilia. To elucidate the role of Bcl-2 family members in the inhibition of eosinophil apoptosis, we examined the expression of the known anti-apoptotic genes Bcl-2, Bcl-xL, and A1, as well as Bax and Bcl-xS, which promote apoptosis in other systems. We show herein that freshly isolated human eosinophils express significant amounts of Bcl-xL and Bax, but only little or no Bcl-2, Bcl-xS, or A1. As assessed by reverse transcription-polymerase chain reaction, immunoblotting, flow cytometry, and immunocytochemistry, we show that spontaneous eosinophil apoptosis is associated with a decrease in Bcl-xL mRNA and protein levels. In contrast, stimulation of the cells with granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin-5 (IL-5) results in maintenance or upregulation of Bcl-xL mRNA and protein levels. Moreover, Bcl-2 protein is not induced by GM-CSF or IL-5 in purified eosinophils. Bcl-2 protein is also not expressed in tissue eosinophils as assessed by immunohistochemistry using two different eosinophilic tissue models. Furthermore, Bcl-xL antisense but not scrambled phosphorothioate oligodeoxynucleotides can partially block the cytokine-mediated rescue of apoptotic death in these cells. These data suggest that Bcl-xL acts as an anti-apoptotic molecule in eosinophils. © 1998 by The American Society of Hematology.


1996 ◽  
Vol 81 (3) ◽  
pp. 977-984
Author(s):  
A E Heufelder ◽  
J R Goellner ◽  
R S Bahn ◽  
G J Gleich ◽  
I D Hay

2014 ◽  
Vol 151 (1_suppl) ◽  
pp. P114-P114
Author(s):  
Todd T. Kingdom ◽  
Sarah A. Gitomer ◽  
Stefan H. Sillau ◽  
Rohit K. Katial ◽  
Vijay R. Ramakrishnan

Ophthalmology ◽  
1991 ◽  
Vol 98 (6) ◽  
pp. 928-932 ◽  
Author(s):  
Hisashi Noguchi ◽  
Gail M. Kephart ◽  
R. Jean Campbell ◽  
James T. Li ◽  
Kristin M. Leiferman ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document