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Dive into the research topics where Teet Pullerits is active.

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Featured researches published by Teet Pullerits.


Allergy | 2010

Growing up on a farm leads to lifelong protection against allergic rhinitis.

Jonas Eriksson; Linda Ekerljung; Jan Lötvall; Teet Pullerits; Göran Wennergren; Eva Rönmark; Kjell Torén; Bo Lundbäck

To cite this article: Eriksson J, Ekerljung L, Lötvall J, Pullerits T, Wennergren G, Rönmark E, Torén K, Lundbäck B. Growing up on a farm leads to lifelong protection against allergic rhinitis. Allergy 2010; 65: 1397–1403.


Allergy | 2007

Effects of pollen and nasal glucocorticoid on FOXP3+, GATA-3+ and T-bet+ cells in allergic rhinitis.

Carina Malmhäll; Apostolos Bossios; Teet Pullerits; Jan Lötvall

Background:  T‐regulatory cells (Treg) affect the balance of TH2 and TH1 cells. Treg, TH2 and TH1 cells are regulated by the FOXP3, GATA‐3 and T‐bet transcription factors respectively. Our aim was to determine the number of FOXP3+, GATA‐3+ and T‐bet+ cells in nasal mucosa in symptom‐free allergic rhinitis (AR) patients vs healthy controls, as well as the effects of natural pollen exposure and concomitant nasal glucocorticoid treatment on these cells.


Clinical & Experimental Allergy | 2005

Increased number of CD34+ cells in nasal mucosa of allergic rhinitis patients: inhibition by a local corticosteroid

Svetlana Sergejeva; Carina Malmhäll; Jan Lötvall; Teet Pullerits

Background Eosinophils develop from CD34+ haematopoietic progenitor cells. Allergen exposure in susceptible individuals is known to induce a local eosinophilic inflammation, but the effect on progenitor cells is much less understood.


Allergy | 1997

Bronchial hyperresponsiveness, epithelial damage, and airway eosinophilia after single and repeated allergen exposure in a rat model of anhydride‐induced asthma

Zhi-Hua Cui; Margareta Sjöstrand; Teet Pullerits; P. Andius; B E Skoogh; Jan Lötvall

Bronchial hyperresponsiveness (BHR) and damage of the epithelium, as well as eosinophilia in the airway wall, induced by trimellitic anhydride (TMA) in sensitized brown Norway rats were studied. Rats were challenged once or seven times with aerosol of TMA conjugated to rat serum albumin (TMA‐RSA) 3 weeks after intradermal TMA sensitization. Airway responsiveness (‐log PC300 of acetylcholine i.v.) was measured 24 h after allergen challenge. Epithelial lesion and eosinophil infiltration in the airway walls were quantified under light microscopy, and TMA‐specific IgE and IgG in serum were evaluated with ELISA. High levels of TMA‐specific IgE and IgG were found in all rats in the sensitized groups compared to nonsensitized groups (P < 0.001). Repeated allergen challenges of 0.03% TMA‐RSA for 7 consecutive days enhanced the level of TMA‐specific IgG, compared to single challenge (P < 0.05). Single allergen challenge of 0.3% TMA‐RSA had a nonsignificant tendency to produce BHR in sensitized rats compared to nonsensitized rats (P=0.06). However, repeated allergen challenges (0.003% and 0.03% TMA‐RSA for 7 consecutive days) produced significant BHR in sensitized rats (P < 0.05). Furthermore, repeated low‐dose (0.003%) TMA‐RSA challenge produced more BHR than a 10 times higher single dose (0.03%) (P < 0.05). Slight damage of the airway epithelium was seen in sensitized and repeat‐challenged groups. However, bronchial eosinophilia was found in the sensitized and single‐challenged groups, but not in nonsensitized nonchallenged, and sensitized repeat‐challenged groups (P < 0.005). We conclude that the brown Norway rat can be sensitized with TMA, and that repeated low‐dose allergen challenges produce slight epithelial damage and BHR which is independent of ongoing eosinophilia in the airway wall.


International Archives of Allergy and Immunology | 2011

Prevalence of Chronic Nasal Symptoms in West Sweden: Risk Factors and Relation to Self-Reported Allergic Rhinitis and Lower Respiratory Symptoms

Jonas Eriksson; Linda Ekerljung; Teet Pullerits; Kenneth Holmberg; Eva Rönmark; Jan Lötvall; Bo Lundbäck

Background: There are few population-based studies on chronic nasal symptoms and little is known about their prevalence and determinants, or their association with allergic rhinitis and asthma. Methods: A questionnaire focused on respiratory symptoms and conditions was mailed in 2008 to 30,000 randomly selected subjects aged 16–75 years in West Sweden, 29,218 could be traced and 18,087 (62%) responded. The questionnaire included questions on self-reported allergic rhinitis, asthma, lower respiratory and nasal symptoms and possible determinants. Results: Nasal congestion was reported by 14.9% and runny nose by 13.1% of subjects. In total, 19.8% had chronic nasal symptoms. Subjects with chronic nasal symptoms had considerably more symptoms from the lower airways compared with nonrhinitic subjects and vice versa. Forty-seven percent of the subjects with chronic nasal symptoms had concurrent self-reported allergic rhinitis. Several hereditary and environmental factors were associated with chronic rhinitis, including family history of asthma [odds ratio (OR) 1.27; 95% confidence interval 1.07–1.50], family history of allergy (OR 1.74; 1.57–1.92) and current smoking (OR 1.39; 1.25–1.54). Further, chronic nasal symptoms were increasingly prevalent with an increasing degree of urbanization. Conclusion: The prevalence of chronic nasal symptoms in West Sweden was found to be high and strongly associated both with self-reported allergic rhinitis and symptoms from the lower airways. Moreover, several risk factors were identified for chronic nasal symptoms, including family history of allergy and asthma and smoking.


Clinical & Experimental Allergy | 2000

Upregulation of nasal mucosal eotaxin in patients with allergic rhinitis during grass pollen season : effect of a local glucocorticoid

Teet Pullerits; Anders Lindén; Lea Praks; Lo Cardell; Jan Lötvall

Allergic rhinitis is a common disease characterized by infiltration of eosinophils into the nasal mucosa during the periods of symptoms. Among chemokines, which attract cells to the site of inflammation, eotaxin is relatively specific for eosinophils.


The Journal of Allergy and Clinical Immunology | 1997

An intranasal glucocorticoid inhibits the increase of specific IgE initiated during birch pollen season.

Teet Pullerits; Lea Praks; Margareta Sjöstrand; Sabina Rak; Bengt-Eric Skoogh; Jan Lötvall

BACKGROUND Recent in vitro findings show that glucocorticoids in combination with IL-4 can induce the synthesis of IgE, indicating that glucocorticoids may promote allergy. OBJECTIVE A double-blind, placebo-controlled study was performed to evaluate the effect of an intranasal glucocorticoid on the levels of birch pollen-specific IgE antibodies in serum from patients with allergic rhinitis. METHODS Eighteen patients with allergic rhinitis received treatment with an intranasal glucocorticoid (beclomethasone dipropionate, 400 microg/day) or placebo for 5 weeks, starting from the beginning of the birch pollen season. Blood samples for anti-birch IgE evaluation were taken before treatment was initiated and at 2 and 5 weeks after the beginning of the study. RESULTS The beclomethasone group (n = 9) had significantly lower symptom scores when compared with the placebo group (n = 9) (0.86 +/- 0.26 vs 2.79 +/- 0.76, p value = 0.01). Both the treatment group and the placebo group showed a trend of an increase in anti-birch IgE levels 2 weeks after the beginning of the treatment (from 33.1 +/- 13.1 kU/L to 44.9 +/- 20.9 kU/L in the beclomethasone group and from 53.2 +/- 18.9 kU/L to 64.1 +/- 22.1 kU/L in the placebo group). Treatment with beclomethasone returned anti-birch IgE levels to baseline by the end of the study, whereas in the placebo group the anti-birch IgE levels continued to increase (final values, 33.1 +/- 11.9 kU/L vs 72.6 +/- 23.2 kU/L, respectively). The change in IgE antibody levels in the placebo group was significantly higher than that in the beclomethasone group. No statistically significant changes in total IgE or soluble CD23 levels were detected. CONCLUSION We conclude that treatment with an intranasal glucocorticoid initiated at the beginning of the pollen season inhibits the induced increase in specific IgE.


Allergy | 2001

Effect of seasonal allergen exposure on mucosal IL-16 and CD4 + cells in patients with allergic rhinitis

Teet Pullerits; Anders Lindén; Carina Malmhäll; Jan Lötvall

Background: CD4+ T cells constitute a major source of cytokines in allergic diseases such as allergic rhinitis. Interleukin (IL)‐16 selectively recruits CD4+ cells.


International Archives of Allergy and Immunology | 1997

Development of Antigen-Specific IgE after Sensitisation with Trimellitic Anhydride in Rats Is Attenuated by Glucocorticoids and Cyclosporin A

Teet Pullerits; Ulf Dahlgren; Bengt-Eric Skoogh; Jan Lötvall

BACKGROUND Trimellitic anhydride (TMA) is a low-molecular-weight compound capable of inducing occupational asthma in man. We have characterized the TMA-induced antibody responses in Brown-Norway rats (BNR) and evaluated the effects of treatment with the glucocorticoid betamethasone or with cyclosporin A (CsA) on this response. METHODS Animals were sensitised by two intradermal injections of 0.1 ml TMA suspended in corn oil, and development of specific antibodies was assessed using ELISA. RESULTS Both IgE and IgG anti-TMA antibodies started to rise between weeks 1 and 3 after immunisation, reached their highest levels 7 weeks after sensitisation with 3% of TMA and then started to decline. Betamethasone and CsA given orally over the time of sensitisation (8 days in total) inhibited the development of specific IgE and IgG anti-TMA antibodies. Betamethasone given 10-17 days after sensitisation attenuated the IgE and IgG antibody responses as well while treatment with CsA after sensitisation had no effect on the production of specific antibodies. Levels of total IgE and IgG were not affected except for a small decrease in total IgE using medium-dose betamethasone after sensitisation. CONCLUSION We conclude that TMA-sensitised BNR develop specific IgE and IgG anti-TMA antibodies, and that glucocorticoids and CsA attenuate this response.


Respiratory Medicine | 2014

Capsaicin cough threshold test in diagnostics.

Teet Pullerits; Ewa Ternesten-Hasséus; Ewa-Lena Johansson; Eva Millqvist

BACKGROUND Among patients with chronic unexplained cough, there is a recognized subgroup with respiratory symptoms induced by environmental irritants like chemicals and odours. The diagnosis of sensory hyperreactivity (SHR) has been suggested for this group of patients and can be made using a tidal breathing capsaicin inhalation test. The aim of the present study was to evaluate the ability of a single-breath, dose-response capsaicin threshold test to discriminate such patients from control subjects. METHODS A total of 46 patients with chronic cough and SHR who had previously shown a positive reaction in accordance with limits set for a tidal breathing capsaicin test were tested once with a single-breath, dose-response capsaicin cough threshold test, assessing capsaicin concentrations to evoke 2 (C2), 5 (C5) or 10 (C10) coughs. Twenty-nine subjectively healthy control subjects were also included and tested with the threshold method. RESULTS Patients had significantly lower C2, C5 and C10 in comparison to controls. From the results among patients and controls, sensitivity and specificity were calculated, and a receiver operating characteristic curve was constructed, showing excellent ability for C5 and C10 to discriminate patients from control subjects. CONCLUSIONS For patients with SHR and chronic cough, capsaicin cough sensitivity was once again confirmed to be increased, in this case, using the single-breath dose-response method. Limits set for cough reactions regarded as more sensitive than normal can be useful in diagnostics and further research. C5 seems to be the best measure to use in research and differential diagnostics.

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Bengt-Eric Skoogh

Sahlgrenska University Hospital

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B E Skoogh

University of Gothenburg

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Ulf Dahlgren

University of Gothenburg

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