P-glycoprotein is a marker of tissue eosinophilia and radiographic inflammation in chronic rhinosinusitis without nasal polyps.
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):684-7. doi: 10.1002/alr.21176. Epub
2013 May 15.P-glycoprotein is a marker of tissue eosinophilia and radiographic inflammation in chronic rhinosinusitis without nasal polyps.1, , , .1Department of Otology and Laryngology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA 02114, USA.AbstractBACKGROUND: P-glycoprotein (P-gp) is a membrane-bound efflux pump that is upregulated in chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) and participates in epithelial cytokine secretion. Eosinophilic CRS (ECRS) shares a similar cytokine profile with CRSwNP and is associated with significant inflammation and poor surgical outcomes. The goal of this study is to determine if P-gp expression is associated with degree of eosinophilia and severity of radiographic inflammation in patients with CRS without polyps (CRSsNP).METHODS: An institutional review board (IRB)-approved study using sinus tissue in 39 steroid-naive patients with CRS. P-gp expression was calculated using quantitative fluorescent immunohistochemistry (Q-FIHC) to generate an epithelial to background staining ratio. Patients were stratified into low and high epithelial expression groups (&3 and ≥3, respectively). Average eosinophils per high powered field (hpf) and Lund-Mackay scores were calculated and compared with P-gp staining ratios using a 2-tailed Student t test.RESULTS: Among the 39 patients, 7 (17.95%) had high P-gp expression ratios (mean ± SD, 4.86 ± 1.33) while 32 (82.05%) had low expression ratios (1.91 ± 0.45). The number of eosinophils/hpf were significantly greater in the high P-gp expression group as compared to the low expression group (62.38 ± 83.69 vs 5.11 ± 10.12, p = 0.0003). The Lund-Mackay scores were significantly greater in the high P-gp expression group as compared to the low expression group (11.86 ± 2.79 vs 6.84 ± 4.19, p = 0.005).CONCLUSION: P-gp is known to be overexpressed in CRSwNP. This study suggests that among patients with CRSsNP, P-gp is similarly overexpressed in those with high tissue eosinophilia and correlates with severity of radiographic inflammation.(C) 2013 The Authors. International Forum of Allergy & Rhinology, published by Wiley Periodicals, Inc., on behalf of ARS-AAOA, LLC.KEYWORDS: Lund-M P- Th1; Th2; eosinophilic ch nasal polyposisPMID:
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External link. Please review our .Eosinophilia is induced in the colon of Th2-sensitized mice upon exposure to locally expressed antigen.
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2007 Apr 12.Eosinophilia is induced in the colon of Th2-sensitized mice upon exposure to locally expressed antigen.1, , , , , , .1Department of Pathology and Molecular Medicine, Center for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada. zhuq@mail.nih.govAbstractEosinophilic inflammation is a feature of a variety of gastrointestinal (GI) disorders including eosinophil-associated GI disorder, allergy, inflammatory bowel disease, and parasite infection. Elucidating the mechanisms of eosinophil infiltration into the GI tract is important to the understanding of multiple disease processes. We hypothesize that eosinophilia in the large intestine (colon) can be induced by an antigen in a host that is associated with Th2-skewed antigen-specific immune responses. To investigate the importance of antigenic triggering, we established polarized antigen-specific Th2 type responses in BALB/c mice, using ovalbumin in conjunction with aluminum hydroxide. Upon challenge at the colonic mucosa through transient (3-4 days) expression of the antigen gene encoded in an adenovirus vector, sensitized animals developed significant subepithelial colonic inflammation, characterized by marked eosinophilic infiltration, and the presence of enlarged and increased numbers of lymphoid follicles. The alterations peaked around day 5 and resolved over the next 5-10 days, and no epithelial cell damage was detected through the entire course. Administration of a control (empty) adenovirus vector did not lead to any pathological changes. These data suggest that colonic eosinophilia can be induced by exposure to an antigen associated with preexisting Th2-skewed responses. Thus the model established here may provide a useful tool to study GI and, in particular, colonic inflammation with respect to underlying mechanisms involved in the recruitment and the immediate function of eosinophils.PMID:
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External link. Please review our .Sputum eosinophilia is more closely associated with airway responsiveness to bradykinin than methacholine in asthma.
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):551-6.Sputum eosinophilia is more closely associated with airway responsiveness to bradykinin than methacholine in asthma.1, , , , , .1Istituto Malattie Apparato Respiratorio, University of Catania, Italy.AbstractHyperresponsiveness of the airways to various spasmogenic stimuli is a characteristic feature of bronchial asthma. However, the association between the different stimuli to which asthmatic airways are hyperresponsive and airways inflammation is not completely understood. We have investigated the relationship between airway inflammation and airway hyperresponsiveness in asthma, as assessed by bronchoprovocation tests to methacholine and bradykinin, two well defined bronchoconstrictor agonists. Sputum induction by hypertonic saline and methacholine and bradykinin challenges were performed in 14 nonsmoking subjects with mild-to-moderate asthma. Airway responsiveness to either agonist did not correlate with sputum neutrophils, lymphocytes, and macrophages. Whilst the absolute number of eosinophilia failed to be significantly related to methacholine responsiveness (r=-0.47; p=0.09), it correlated markedly and significantly with provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second (r=0.72; p&0.01). When expressed as % of total cell counts, sputum eosinophils correlated with both types of responsiveness (r=-056; p=0.04 and r=-0.76, p&0.001, respectively). Although the concentration of eosinophil cationic protein (ECP) in the sputum correlated with the absolute numbers of eosinophils (r=0.62; p&0.02), no correlation was found between ECP levels and the airway responsiveness to any of the agonists tested. In subjects with mild-to-moderate asthma, airway responsiveness to bradykinin is more strongly associated with the magnitude of eosinophilic inflammation in the airways than methacholine. This finding underlines the selectivity of diverse agonists in assessing airway hyperresponsiveness and cellular inflammation in asthma.PMID: 9762778
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Eosinophilia (e-o-sin-o-FIL-e-uh) is a higher than normal level of eosinophils. Eosinophils are a type of disease-fighting white blood cell.
You can have high levels of eosinophils in your blood (blood eosinophilia). High levels of eosinophils may also occur in your body's tissues at the site of an infection or inflammation (tissue eosinophilia).
Tissue eosinophilia may be found in samples taken during an exploratory procedure or in samples of certain fluids, such as mucus released from nasal tissues. If you have tissue eosinophilia, the level of eosinophils in your bloodstream is likely normal.
Blood eosinophilia may be detected with a blood test, usually as part of a complete blood count. A count of more than 500 eosinophils per microliter of blood is generally considered eosinophilia in adults. A count of more than 1,500 eosinophils per microliter of blood that lasts for several months is called hypereosinophilic syndrome.
Weller PF. Approach to the patient with eosinophilia. /home. Accessed July 26, 2013.
Eosinophilia. The Merck Manuals: The Merck Manual for Healthcare Professionals. /professional/hematology_and_oncology/eosinophilic_disorders/eosinophilia.html#v973281. Accessed July 26, 2013.
Kliegman RM, et al. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, Pa.: Saunders E 2011. . Accessed July 30, 2013.
CBC with differential, blood. Mayo Medical Laboratories. /test-catalog/Clinical+and+Interpretive/9109. Accessed July 26, 2013.
Roufosse F, et al. Clinical manifestations, pathophysiology, and diagnosis of the hypereosinophilic syndromes. /home. Accessed July 26, 2013.
Ustianowski A, et al. Eosinophilia in the returning traveler. Infectious Disease Clinics of North America. .
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