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  • Recently it has been shown that among the

    2020-02-14

    Recently, it has been shown that among the ELR (+) chemokines mentioned above, particularly IL-8 induces neutrophil migration via CXCR-1 chemokine receptor. For example, Godaly et al. [18] reported the potent role of CXCR-1 chemokine receptor in the process of neutrophil migration across epithelial cell layers. Furthermore, our recent work has shown that the tail of CXCR-1 chemokine receptor was responsible for β1 integrin-dependent cell migration stimulated by IL-8 in mononuclear cell lines [9]. Chemokines are involved not only in the migration of neutrophils but also their prolonged accumulation at the site of inflammation. Chemokine receptors that play a pivotal role in the process of neutrophil accumulation (holding) are not very well defined. Stimulation of neutrophils with LPS and TNF-α has been shown to down-regulate the expression of CXCR-1 and CXCR-2 [19], [20] while shown to up-regulate the receptors for CC chemokines such as CCR1, CCR2, CCR3, CCR5, CCR6 [21], [22], [23]. Histopathological studies investigating the role of chemokine receptors in various inflammatory diseases proposed a more potent role for CXCR-1 chemokine receptor in the course of neutrophil long lasting accumulation. Using monoclonal antibodies, Williams et al. [24] studied the distribution of CXCR-1 and CXCR-2 chemokine receptor in the resection specimens of cases having acute appendicitis and ulcerative colitis and found more marked up-regulation of CXCR-1 chemokine receptor expression as compared to CXCR-2. Receptor expressions of lymphocytes, macrophages and other inflammatory nrf2 inhibitor were also examined in that study in addition to those of the neutrophils. Likewise, Ohtani et al. [25] demonstrated increased surface CXCR-1 chemokine receptor expression of neutrophils in the pathological specimens obtained from patients with ulcerative colitis, Crohn\'s disease, and chronic gastritis associated with Helicobacter pylori infection. Additionally, it has been revealed that CXCR-2 chemokine receptor is down-regulated in patients with severe sepsis, yet CXCR-1 remains functional with normal cell surface expression [26]. Contrary to the studies suggesting a critical role for CXCR-1 chemokine receptors in the migration and prolonged accumulation of neutrophils, Podolin et al. [27] reported that a potent and selective antagonist of CXCR-2 chemokine receptor inhibits models of acute and chronic arthritis in the rabbit. Despite the existence of several studies investigating chemokine receptor expression of monocytes and lymphocytes in the synovial fluid of patients with inflammatory arthritides [28], [29], [30], [31], [32], [33], [34], only a limited number of studies have been found regarding the chemokine receptor expression of neutrophils in similar settings. Galligan et al. [35] reported an up-regulated expression of an orphan chemokine receptor, CCRL2, on synovial neutrophils of RA patients and proposed a possible role for this receptor in the pathogenesis of RA. In addition, significant reduction in the surface expression of CXCR-1 and CXCR-2 chemokine receptor on SFN as compared to the peripheral blood was shown by Brühl et al. [36]. We were not able to find any literature (previous data) that may help to explain our finding of an increased CXCR-1 receptor expression in the PBN of patients with RA. On the other hand, increased CXCR-1 expression in patients with BD can be attributed to the nature of BD itself, which is considered to be a neutrophil mediated disease and characterized by increased numbers of activated neutrophils. The results of the present study are in accordance with those of Brühl et al. [36] as showing a decreased expression of CXCR-1 chemokine receptor in the synovial fluid of the patients. The down-regulation of surface CXCR-1 chemokine receptors in the SFN may probably the consequence of highly increased gradient of synovial fluid chemokines when compared with those of the peripheral blood.