Blood eosinophil count as risk factor for relapse in acute asthma

Janson, Christer; Herala, Merja

doi:10.1016/s0954-6111(06)80223-4

Cited by 24 publications

(13 citation statements)

References 8 publications

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“…Enhanced numbers of blood eosinophils per se is proposed to be a risk factor in asthma [ 4]. In our study, the absolute number of peripheral blood eosinophils in the control subjects was within normal range (≤ 400 PBE/μL blood, Division of Clinical Chemistry, Karolinska Hospital) both before and after allergen provocation.…”

Section: Discussionsupporting

confidence: 58%

“…An increased influx of eosinophils has been observed both in allergic and nonallergic asthma [ 1, 2]. In symptomatic asthma enhanced number of eosinophils has been found in peripheral blood [ 3, 4], sputum [ 5], bronchoalveolar lavage fluid (BAL) [ 6, 7] and the bronchial wall [ 8, 9]. The severity of eosinophilia in airway hyperresponsiveness and asthma suggested that eosinophils contribute to the development of asthmatic symptoms [ 10].…”

Section: Introductionmentioning

confidence: 99%

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Increased levels of IL‐5 positive peripheral blood eosinophils and lymphocytes in mild asthmatics after allergen inhalation provocation

Halldén

Hellman

Grönneberg

et al. 1999

Clin Experimental Allergy

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Background In allergic inflammation eosinophils and TH2‐like lymphocytes are supposed to be the major effector cells and considered to contribute as cellular source of the key cytokine interleukin (IL)‐5. Objective The purpose of this study was to enable detection of IL‐5 containing leucocytes and to investigate whether the number of these cells in the blood circulation differed between healthy and asthmatics before and after allergen provocation. Methods The distribution of intracellular IL‐5 in human peripheral blood eosinophils (PBE) and lymphocytes (PBL) has been investigated using fixation and cell membrane permeabilization with octyl‐glucopyranoside, the FOG‐method, and flow cytometry. The intracellular staining was performed on leucocytes without any prior purification and in vitro stimulation. The specificity of IL‐5 binding to intracellular compartment of both PBE and PBL was confirmed by complete inhibition with human recombinant IL‐5. Results Preformed intracellular IL‐5 was detected in the main population of PBE (> 70%) in both healthy individuals and asymptomatic patients. Moreover, preformed intracellular IL‐5 was also detected in 4.8% and 2.4% of PBL from healthy individuals and asymptomatic patients, respectively. There was a correlation between the absolute number of PBE and IL‐5 positive PBE. In patients with pollen‐related asthma, the number of IL‐5 positive PBE and PBL increased significantly 24 h after an allergen inhalation provocation (P < 0.05). In the healthy control group no differences regarding IL‐5 positive PBE and PBL were obtained pre‐ and post‐allergen challenge. Conclusions In patients with mild allergic asthma, but not in healthy individuals, allergen provocation induces an increased absolute number of IL‐5 positive PBE and PBL. The reason for the relatively high number of IL‐5 positive PBL is unclear, but a plausible explanation might be that other lymphocyte subsets besides CD4+ TH2 can produce IL‐5. However, enumeration of IL‐5 positive leucocytes may be used as an activity marker and also be a useful tool in monitoring the inflammation in asthma.

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Section: Discussionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Increased levels of IL‐5 positive peripheral blood eosinophils and lymphocytes in mild asthmatics after allergen inhalation provocation

Halldén

Hellman

Grönneberg

et al. 1999

Clin Experimental Allergy

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“…In particular, IL5 and IL13 concentrations were approximately eight and three-fold higher in females than males, respectively. Blood eosinophilia has been shown to be a risk factor in acute asthma (Janson and Herala, 1992); IL13 is a key cytokine in the pathogenesis of allergic asthma (Grunig et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Gender Differences in the Allergic Response of Mice Neonatally Exposed to Environmental Tobacco Smoke

Seymour

Friebertshauser

Peake

et al. 2002

Journal of Immunology Research

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Exposure to environmental tobacco smoke (ETS) has been shown to increase allergic sensitization and reactivity and there has been some suggestion that the influence of ETS on the allergic response is dissimilar in males and females. It is to be determined whether gender differences exist in the IgE response to ovalbumin (OVA) sensitization following ETS exposure from the neonatal period through adulthood. To address this thesis, we examined gender differences in OVA sensitization of BALB/c mice housed from birth through adulthood under smoking and nonsmoking conditions. At 6 weeks of age (day 0) all mice were injected i.p. with OVA in aluminum hydroxide adjuvant followed by three 20 min exposures to 1% aerosolized OVA between day 14 and 80. There were significantly (p<0.05) more total and OVA specific IgE and IgG1 in the serum of females compared to males. Moreover, these sex responses, along with eosinophilia, were further enhanced in mice exposed to ETS. There were also significantly more IgE positive cells in the lungs of female, but not male, mice exposed to ETS compared with ambient air (p<0.05). There was also an elevation of Th2 cytokines (IL4, IL5, IL10, and IL13) after re-stimulation of lung homogenates following ETS exposure. These data demonstrate that female animals are significantly more susceptible than males to the influence of ETS on the allergic response.

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“…Briefly, the rats were immunized by i.p. injection with 1 ml emulsion solution containing 1 mg OVA (Sigma-Aldrich, St. Louis, MO) and 50 mg Al (OH) 3 (Pierce Biotechnology, Rockford, IL). For screening the expression of PRMTs in lungs, 16 rats were divided into control group and AIPI group.…”

Section: Methodsmentioning

confidence: 99%

“…Eosinophils, which play an important role in asthma, are recruited into the lung during both acute and chronic pulmonary inflammation (2,3). Accumulating evidence has demonstrated that the eosinophil infiltration into lungs both in animal models and human diseases can be attributed to the high expression of eotaxins (4,5), and increased IL-4 production is associated with eosinophilia and promotes eosinophilic inflammation through induction of eotaxin-1 (6,7).…”

mentioning

confidence: 99%

Upregulated Protein Arginine Methyltransferase 1 by IL-4 Increases Eotaxin-1 Expression in Airway Epithelial Cells and Participates in Antigen-Induced Pulmonary Inflammation in Rats

Sun

Yang

Zhong

et al. 2012

The Journal of Immunology

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Protein arginine methyltransferases (PRMTs), catalyzing methylation of both histones and other cellular proteins, have emerged as key regulators of various cellular processes. This study aimed to identify key PRMTs involved in Ag-induced pulmonary inflammation (AIPI), a rat model for asthma, and to explore the role of PRMT1 in the IL-4–induced eosinophil infiltration process. E3 rats were i.p. sensitized with OVA/alum and intranasally challenged with OVA to induce AIPI. The expressions of PRMT1–6, eotaxin-1, and CCR3 in lungs were screened by real-time quantitative PCR. Arginine methyltransferase inhibitor 1 (AMI-1, a pan-PRMT inhibitor) and small interfering RNA–PRMT1 were used to interrupt the function of PRMT1 in A549 cells. In addition, AMI-1 was administrated intranasally to AIPI rats to observe the effects on inflammatory parameters. The results showed that PRMT1 expression was mainly expressed in bronchus and alveolus epithelium and significantly upregulated in lungs from AIPI rats. The inhibition of PRMTs by AMI-1 and the knockdown of PRMT1 expression were able to downregulate the expressions of eotaxin-1 and CCR3 with the IL-4 stimulation in the epithelial cells. Furthermore, AMI-1 administration to AIPI rats can also ameliorate pulmonary inflammation, reduce IL-4 production and humoral immune response, and abrogate eosinophil infiltration into the lungs. In summary, PRMT1 expression is upregulated in AIPI rat lungs and can be stimulated by IL-4. Intervention of PRMT1 activity can abrogate IL-4–dependent eotaxin-1 production to influence the pulmonary inflammation with eosinophil infiltration. The findings may provide experimental evidence that PRMT1 plays an important role in asthma pathogenesis.

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Blood eosinophil count as risk factor for relapse in acute asthma

Cited by 24 publications

References 8 publications

Increased levels of IL‐5 positive peripheral blood eosinophils and lymphocytes in mild asthmatics after allergen inhalation provocation

Increased levels of IL‐5 positive peripheral blood eosinophils and lymphocytes in mild asthmatics after allergen inhalation provocation

Gender Differences in the Allergic Response of Mice Neonatally Exposed to Environmental Tobacco Smoke

Upregulated Protein Arginine Methyltransferase 1 by IL-4 Increases Eotaxin-1 Expression in Airway Epithelial Cells and Participates in Antigen-Induced Pulmonary Inflammation in Rats

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