001, respectively) (Table 1) Moreover, in NRs, plasma concentra

001, respectively). (Table 1). Moreover, in NRs, plasma concentration of CCL17 (96 pg/ml; 95%CI 82–110 pg/ml) was significantly greater KU-57788 mouse than in HCs (P < 0.001) but was significantly less than in Rs (P = 0.01), while baseline plasma concentration of CX3CL1 in NRs (357 pg/ml; 95%CI 300–415 pg/ml) was greater than in HCs (P = 0.003) but did not differ from that of Rs (P = 0.982). The baseline plasma concentrations of CCL2 did not differ

significantly between Rs, NRs and HCs. In Rs, allergen challenge resulted in increase in plasma CCL17 and CCL2 concentrations which at T24 were 296 pg/ml; 95%CI 180–398 pg/ml (P < 0.001) and 131 pg/ml; 95% CI 109–154 pg/ml (P < 0.001), respectively. No significant difference SB203580 purchase was seen between the mean plasma concentrations of CX3CL1 at T0, T6 or T24 (Fig. 4). In NRs, plasma concentration of neither of the chemokine studied changed over a period of 24-h observation after allergen challenge (not shown). Moreover, at T24, only plasma concentration of CCL17 correlated inversely with the number of circulating CD14++ CD16+ cells (r = −0.58, 95% CI −0.835 to −0.12, P = 0.018). Subsequently, we analysed the expression of chemokine receptor CCR4 on

individual PBM subsets. The mean expression of CCR4 on CD14++ CD16+ PBMs (8.32 FU; 95%CI 7.85–8.78) was significantly greater than on CD14+ CD16++ PBMs (7.11 FU; 95%CI 6.8–7.42 FU; P = 0.001) which in turn was significantly greater than on CD14++ CD16− PBMs (6.08 FU; 95%CI 5.74–6.42 FU; P = 0.001) (Fig. 5). There was no significant difference in expression of CCR4 on individual PBM subsets between HCs, NRs and Rs. This is the first study which demonstrates different changes in the number of individual PBM subsets in allergic asthma patients in response to bronchial allergen challenge. Moreover, in our report, three monocyte subsets separated based on staining with anti-CD14

and anti-CD16 antibodies have been analysed. Previous studies focused mainly on two monocyte subpopulations divided solely on the basis of the presence or absence of CD16 [17–20]. Elevated number of circulating CD16+ SDHB monocytes has been reported in asthma [17] but also in other inflammatory diseases such as rheumatoid arthritis [18], tuberculosis [19] or sepsis [20]; however, no further subdivision of the population has been performed. Distinguishing CD14++ CD16+ from CD14+ CD16++ among CD16+ monocytes is justified not only from morphological but also from functional point of view [7]. Interestingly, in the current study, we have demonstrated that in allergic asthma patients, elevated number of circulating CD16+ monocytes is because of expansion of the CD14++ CD16+ subset. The current study extends our previous observations reporting on elevated number of CD14++ CD16+ monocytes in more severe asthmatic patients [6].

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