Abstract
The goal of our study was to assess the chemotactic activity for eosinophils (ECA) and neutrophils (NCA) and histamine releasing activity (HRA) in crude supernatants of mononuclear cells in monosensitized atopic asthmatics and healthy controls. Chemotactic activity for ECA and neutrophils was measured in supernatants of cultured mononuclear cells with modified Boyden's chamber and HRA was assessed on healthy donor basophils. With respect to ECA generation two distinct subgroups of subjects were distinguished: releasers [ECA (+)] and non-releasers [ECA (-)]. In atopic and non-atopic ECA (+) the mean ECA index was 3.78 +/- 0.49 and 2.47 +/- 0.27 respectively (P > 0.05). Supernatants from the remaining subjects (seven of 22 atopic and five of 11 non-atopic) did not express ECA, but revealed significant inhibitory activity for chemokinesis of eosinophils (mean chemotactic index 0.25 +/- 0.16 and 0.48 +/- 0.22 for atopic and non-atopic non-releasers respectively). Stimulation with antigen of MNC from atopic and with PHA from non-atopic ECA (-) restored cells ability to release ECA. Sephadex gel chromatography revealed that supernatants of MNC contained chemotactic and chemokinesis inhibitory activity in different fractions. The spontaneous productions of NCA and HRA by mononuclear cells was similar in ECA releasers and non-releasers, although the HRA was higher following stimulation with PHA in the non-atopic ECA (+) subgroup. Our study demonstrated, for the first time, that MNC are capable of generating not only chemotactic activity but also chemokinesis inhibitory activity for eosinophils.
Highlights
Bronchial asthma is a chronic inflammatory proce ss, charac te rize d by the influx and acc umulation of eosinophils, ne utrophils, lymphocyte s and monocytes /mac rop hages in the airw ay mucosa.[1]
Our earlier studies demonstrated the pre sence of eosinophils che motac tic ac tivity (ECA) in the se rum of patients w ith atopic asthma as w e ll as che motac tic ac tivity for ne utrophils (NCA ) in nasal lavage in patie nts suffering from p ollinosis.[5,6]
The release of ECA by MNC w as doc ume nted in several studies[27,28] to our know le dge this is the first study reporting the release of inhibitory activity tow ards e osinophil chemokine s
Summary
Bronchial asthma is a chronic inflammatory proce ss, charac te rize d by the influx and acc umulation of eosinophils, ne utrophils, lymphocyte s and monocytes /mac rop hages in the airw ay mucosa.[1] An inc re ased number of eosinophils w as observed in bronchial muc osa and in bronchio-alve olar lavage (BAL) in patie nts w ith seasonal and pere nnial asthma.[2] The e osinophilic influx afte r allerge n provocation is acc ompanie d by the inc rease of eosinophils che motac tic ac tivity (ECA) in BAL.[3,4] natural ex posure to allerge n induce s the increase of the ECA in bronchoalve olar lavage and in se rum.[3] Our earlier studies demonstrated the pre sence of ECA in the se rum of patients w ith atopic asthma as w e ll as che motac tic ac tivity for ne utrophils (NCA ) in nasal lavage in patie nts suffering from p ollinosis.[5,6] These data sugge st that mechanisms initiate d as a response to alle rgen leading to release of chemotactic molecules, w hich are responsible for the selec tive influx of eosinophils to the lungs
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