RANTES in Exhaled Breath Condensate of Allergic Asthma Patients with Exercise-Induced Bronchoconstriction

Ziętkowski, Ziemowit; Skiepko, Roman; Tomasiak-Lozowska, M M; Mroczko, Barbara; Szmitkowski, Maciej; Bodzenta-Łukaszyk, Anna

doi:10.1159/000264923

Cited by 22 publications

(10 citation statements)

References 96 publications

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“…R2 peptide also prevented airway tissue remodelling by reducing the increased goblet cell hyperplasia, collagen deposition and imbalance of MMPs and TIMPs. The migration of inflammatory cells from blood into the airway occurs through binding to specific adhesion molecules such as VCAM-1 and chemokines such as CCL5 and IL-8 (Berkman et al, 1996;Zietkowski et al, 2009). VCAM-1 expression is enhanced by Th2-mediated cytokines such as IL-4, IL-13 and TNF-a (Sriramarao et al, 2000;Wills-Karp and Karp, 2004).…”

Section: Discussionmentioning

confidence: 99%

Anti‐inflammatory effects of the R2 peptide, an inhibitor of transglutaminase 2, in a mouse model of allergic asthma, induced by ovalbumin

Kim

Park

Hong

et al. 2010

British J Pharmacology

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BACKGROUND AND PURPOSETransglutaminase 2 (TGase 2) expression is increased in inflammatory diseases, and TGase 2 inhibitors block these increases. We examined whether the R2 peptide inhibited the expression of TGase 2 in a mouse model of inflammatory allergic asthma. EXPERIMENTAL APPROACHC57BL/6 mice were sensitized and challenged by ovalbumin (OVA) to induce asthma. OVA-specific serum IgE and leukotrienes (LTs) levels were measured by enzyme-linked immunosorbent assay. Recruitment of inflammatory cells into bronchoalveolar lavage (BAL) fluid or lung tissues and goblet cell hyperplasia were assessed histologically. Airway hyperresponsiveness was determined in a barometric plethysmographic chamber. Expression of TGase 2, eosinophil major basic protein (EMBP), the adhesion molecule vascular cell adhesion molecule-1, Muc5ac and phospholipase A2 (PLA2) protein were determined by Western blot. Expression of mRNAs of Muc5ac, cytokines, matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) were measured by reverse transcriptase-polymerase chain reaction and nuclear factor-kB (NF-kB) by electrophoretic mobility shift assay. KEY RESULTSR2 peptide reduced OVA-specific IgE levels; the number of total inflammatory cells, macrophages, neutrophils, lymphocytes and eosinophils in BAL fluid and the number of goblet cells. Airway hyperresponsiveness, TGase 2 and EMBP levels, mRNA levels of interleukin (IL)-4, IL-5, IL-6, IL-8, IL-13, RANTES, tumour necrosis factor-a, and MMP2/9, Muc5ac, NF-kB activity, PLA2 activity and expressions, and LT levels in BAL cells and lung tissues were all reduced by R2 peptide. R2 peptide also restored expression of TIMP1/2. CONCLUSION AND IMPLICATIONSR2 peptide reduced allergic responses by regulating NF-kB/TGase 2 activity in a mouse model of allergic asthma. This peptide may be useful in the treatment of allergic asthma. AbbreviationsBAL, bronchoalveolar lavage; ELISA, enzyme-linked immunosorbent assay; EMBP, eosinophil major basic protein; EMSA, electrophoretic mobility shift assay; MMP, matrix metalloproteinase; NF-kB, nuclear factor-kappa B; OVA, ovalbumin; PAS, periodic acid-Schiff; PBS, phosphate buffered saline; PLA2, phospholipase A2; RT-PCR, reverse transcriptase-polymerase chain reaction; TGase 2, transglutaminase 2; TIMP, tissue inhibitor of matrix metalloproteinase BJP British Journal of Pharmacology

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Section: Discussionmentioning

confidence: 99%

Anti‐inflammatory effects of the R2 peptide, an inhibitor of transglutaminase 2, in a mouse model of allergic asthma, induced by ovalbumin

Kim

Park

Hong

et al. 2010

British J Pharmacology

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“…EIA and EIB are usually defined on the basis of a fall of 1 10% from baseline FEV 1 after a standardized exercise challenge test [6] . The pathogenesis of EIA and EIB remains elusive, although evidence points to dehydration of the airways with eosinophil and mast cell degranulation as central mechanisms behind the phenomenon [7][8][9] , increasing both bronchial muscle constriction and blood vessel dilatation. The latter could be the explanation for an increase in EBT and would possibly be even more pronounced in subjects with concomitant airway inflammation.…”

Section: Introductionmentioning

confidence: 99%

Exhaled Breath Temperature Increases after Exercise in Asthmatics and Controls

et al. 2012

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Background: Exhaled breath temperature (EBT) has been suggested as a marker of airway inflammation in asthma. Objectives: The aim of the present study was to investigate EBT in asthmatic subjects compared to healthy controls after an exercise challenge test, and in subjects with exercise-induced bronchoconstriction compared to subjects without, and to compare with body temperatures. Methods: A total of 21 healthy controls and 20 asthmatics were included. Forced expiratory volume in 1 s (FEV1), EBT and oral, axillary and auricular temperatures were measured before and after an exercise challenge test. Results: FEV1 % predicted (%p) was significantly lower in asthmatic subjects compared to healthy controls at all time points after exercise. The largest drop in FEV1%p correlated with EBT after 5 min. EBT increased markedly 5 min after exercise and remained high for at least 60 min. In asthmatics whose FEV1 dropped by >10%, EBT was higher after 60 min compared to the remaining asthmatics. EBT correlated with oral temperature at all time points after exercise, with axillary temperature only at 15, 30 and 60 min, and not at all with auricular temperature. Conclusions: EBT is increased after exercise, and elevated EBT correlated with a drop in FEV1%p. The immediate increase in EBT did not differ between asthmatics and controls but remained elevated in the asthmatics whose FEV1 dropped by >10%, indicating a different vascular response.

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“…In our previous studies we observed that in asthmatic patients, as a consequence of postexercise bronchoconstriction, increased expression of RANTES in the airways occurs [8]. This process, by promoting the migration and activation of inflammatory cells including eosinophils, may play an important role in upregulation of the airway inflammation observed after EIB in asthmatic patients.…”

Section: Introductionmentioning

confidence: 95%

Eotaxin in Exhaled Breath Condensate of Allergic Asthma Patients with Exercise-Induced Bronchoconstriction

et al. 2011

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Background: Eosinophils are the key inflammatory cells in asthma, and more and more evidence suggests their crucial role in exercise-induced bronchoconstriction (EIB). Eotaxin, as the most important chemotactic factor for eosinophils, plays an important role in the pathogenesis of asthma. Objectives: The aim of the study was to evaluate the changes in eotaxin levels in exhaled breath condensate (EBC) following intensive exercise in allergic asthmatics. Methods: The study was performed in a group of 27 asthmatics (17 with EIB, 13 without EIB) and 9 healthy volunteers. Changes induced by intensive exercise in the concentrations of eotaxin in EBC during the 24 h after an exercise test were assessed. The possible correlations of these measurements with the results of other tests commonly associated with eosinophilic airway inflammation were also determined. Results: In asthmatic patients with EIB, a statistically significant increase in eotaxin concentrations in EBC collected during the first 24 h after an exercise test – with maximal increase after 6 h – was revealed. A statistically significant correlation between the maximum increase in eotaxin concentrations in EBC after exercise, and an increase in either serum eosinophil cationic protein or F_ENO 24 h after exercise in the group of asthmatics with EIB, was observed. Conclusions: Our results confirm connections between EIB and airway eosinophilic inflammation. The increase of eotaxin in asthmatic airways, by promoting the migration and activation of eosinophils, may play an important role in upregulation and sustaining of the airway inflammation observed in EIB in asthmatic patients.

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RANTES in Exhaled Breath Condensate of Allergic Asthma Patients with Exercise-Induced Bronchoconstriction

Cited by 22 publications

References 96 publications

Anti‐inflammatory effects of the R2 peptide, an inhibitor of transglutaminase 2, in a mouse model of allergic asthma, induced by ovalbumin

Anti‐inflammatory effects of the R2 peptide, an inhibitor of transglutaminase 2, in a mouse model of allergic asthma, induced by ovalbumin

Exhaled Breath Temperature Increases after Exercise in Asthmatics and Controls

Eotaxin in Exhaled Breath Condensate of Allergic Asthma Patients with Exercise-Induced Bronchoconstriction

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