Lung accumulations of eosinophil granulocytes after exposure to cornstarch glove powder

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336

249

Exosomes are 30-100 nm diameter vesicles formed by inward budding of endosomal compartments and are produced by several cell types, including T-cells, Bcells and dendritic cells (DC)s. Exosomes from DCs express major histocompatibility complexes (MHC) class I and II, and co-stimulatory molecules on their surface, and can induce antigen-specific activation of T-cells.The aims of the present study were to investigate for the presence of exosomes in bronchoalveolar lavage fluid (BALF) from healthy individuals, and to establish if these exosomes bear MHC and co-stimulatory molecules.The authors analysed BALF taken from seven healthy volunteers and used exosomes from monocyte-derived DC (MDDC) cultures as a reference. After ultracentrifugation, exosomes were bound to anti-MHC class II coated magnetic beads and analysed by flow cytometry and electron microscopy.The authors report for the first time that exosomes are present in BALF. These exosomes are similar to MDDC derived exosomes as they express MHC class I and II, CD54, CD63 and the co-stimulatory molecule CD86.The results demonstrate that exosomes are present in the lung, and since they contain both major histocompatibility complex and co-stimulatory molecules it is likely that they are derived from antigen presenting cells and might have a regulatory role in local immune defence. Eur Respir J 2003; 22: 578-583.

Section: Bronchoalveolar Lavage Fluid Cell Countssupporting

confidence: 82%

Exosomes with major histocompatibility complex class II and co-stimulatory molecules are present in human BAL fluid

Admyre¹,

Grünewald²,

Thyberg³

et al. 2003

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249

“…Moreover, healthy individuals exposed to starch showed dramatic signs of lung-accumulated eosinophils after exposure, eosinophils sometimes making up as much as 30% of all BAL fluid cells [21]. The increase in eosinophil numbers correlated with elevated levels of ECP, indicating eosinophil activation on site after exposure [21].…”

Section: Discussionmentioning

confidence: 97%

Accumulation of eosinophils and T-lymphocytes in the lungs after exposure to pinewood dust

Gripenbäck

Lundgren²,

Eklúnd³

et al. 2005

Exposure to wood dust within the woodworking industry has been shown to cause a variety of respiratory disorders. The aim of this study was to investigate the cellular effects in bronchoalveolar lavage (BAL) fluid and peripheral blood from healthy individuals exposed to pinewood dust. Eleven healthy volunteers were exposed to pinewood dust for 1 h in a whole-body exposure chamber. BAL fluid and blood cells were differentially counted and the expression of activation, adhesion and subset markers on alveolar macrophages and T-lymphocytes was determined 2-6 weeks before and 20 h after the exposure. Following pinewood dust exposure, the total BAL fluid cell concentration increased from 81.4 (64.1-97.5) x 10(6) cells x L(-1) (median (interquartile range)) to 195.3 (154.6-341.2) x 10(6) cells x L(-1). The BAL fluid T-lymphocyte concentration increased from 3.8% (3.5-6.5%) to 7.6% (4.9-11.2%), and BAL fluid eosinophil concentration from 0.0% (0.0-0.2%) to 1.8% (0.6-3.5%). Inhalation of pinewood dust leads to the recruitment of inflammatory cells to the airways of healthy individuals. The increase in numbers of eosinophils, T-lymphocytes and mast cells, i.e. cells of crucial importance to airway inflammation, in the lungs may be related to the increased risk of developing respiratory disorders among woodworkers.

“…of the allergen-carrying glove powder consisting of cornstarch. GRUNEWALD et al [32] showed that inhalation of cornstarch glove powder leads to subclinical inflammation in the airways in previously unexposed subjects.…”

Section: Discussionmentioning

confidence: 99%

Latex allergen exposure increases exhaled nitric oxide in symptomatic healthcare workers

Baur

Barbinova²

2005

The objective of this study was to investigate the clinical and diagnostic impact of baseline exhaled nitric oxide (eNO) levels and latex allergen-induced eNO changes in different healthcare worker groups.Healthcare workers, 31 latex-sensitised and 14 nonsensitised, underwent occupational-type challenge tests with powdered allergenic latex gloves.Sensitised as well as nonsensitised healthcare workers developed a significant eNO increase 1 h after challenge. Conversely, only latex-sensitised employees showed a significant eNO increase 22 h after challenge, which showed a significant relationship with bronchial obstruction (specific airway resistance changes). However, there was no difference in either baseline eNO level or eNO increase after 22 h between asthmatic (n513) and rhinitic only (n520) responders. The specificity and sensitivity of a 50% eNO increase after 22 h in responders were 100 and 56%, respectively.These results support the assumption that the whole respiratory tract is involved in a combined allergic rhinitis and asthma syndrome. Smoking healthcare workers showed reduced baseline exhaled nitric oxide levels, but, as shown for the first time, an allergen-induced exhaled nitric oxide increase comparable to that of nonsmokers. Corticosteroid therapy inhibited the allergeninduced exhaled nitric oxide change but not the clinical response in the challenge test. These findings suggest that cigarette smoke and corticosteroids initiate distinct molecular mechanisms influencing nitric oxide concentrations in the airways. KEYWORDS: Allergy, bronchial asthma, latex, nitric oxide E xhaled nitric oxide (eNO) has been described as a marker of allergic airway inflammation in both rhinitic and asthmatic subjects [1][2][3][4][5][6][7]. eNO levels may be elevated in patients before asthmatic symptoms develop [8,9]. HENRIKSEN et al. [8] and GRATZIOU et al.[9] observed a seasonal rise in eNO levels in pollensensitised subjects with and without rhinitic and/or asthmatic symptoms, with a tendency towards increased concentrations in symptomatic subjects.Despite the considerable number of publications and results indicating relations between baseline eNO level and/or eNO changes on the one hand and symptoms [9][10][11], bronchial hyperresponsiveness [12,13] and inflammatory parameters of the airways [14] on the other, the clinical role of eNO measurements has not been exactly defined. Moreover, the relation between eNO levels and eNO changes following laboratory allergen challenge has so far rarely been compared between subjects with rhinitic and those with asthmatic responses.The present hypothesis is that allergen-induced eNO increases have a clinical and diagnostic impact. Considering the influence of possible confounding factors such as atopy, smoking and corticosteroid therapy, it was investigated whether, in different patient subgroups, baseline eNO concentrations, as well as eNO changes, are associated with: 1) latex-specific immunoglobulin (Ig) E and skin-prick test responses; and 2) clinical responses...