The cytokine-driven regulation of secretoglobins in normal human upper airway and their expression, particularly that of uteroglobin-related protein 1, in chronic rhinosinusitis

abstract: ...Background The involvement of secretoglobins (SCGBs) other than SCGB1A1 (Clara cell 10-kDa protein, CC10) in human airway diseases remains unexplored. Among those SCGBs, SCGB3A2 (uteroglobin-related protein 1, UGRP1) is particularly interesting, given its structure and function similarities with SCGB1A1 (CC10). The aim of this study was to investigate the expression regulation of SCGBs other than SCGB1A1 (CC10) in human upper airway, and their potential involvement, particularly that of SCGB3A2 (UGRP1), in chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP). Methods Eight SCGB family members including SCGB3A2 (UGRP1), SCGB1C1 (ligand binding protein RYD5), SCGB1D1 (lipophilin A), SCGB1D2 (lipophilin B), SCGB1D4 (interferon- inducible SCGB), SCGB2A1 (mammaglobin 2), SCGB2A2 (mammaglobin 1), and SCGB3A1 (uteroglobin-related protein 2) were studied. The regulation of SCGBs mRNA expression in normal nasal mucosa by proinflammatory, Th1, and Th2 cytokines was studied through nasal explant culture. SCGBs mRNA expression levels in CRSsNP and CRSwNP patients and controls were compared. The mRNA levels were detected by means of quantitative reverse transcriptase-polymerase chain reaction. The protein expression of SCGB3A2 (UGRP1) was analyzed using immunohistochemistry. Results The expression of SCGBs except SCGB1D2 (lipophilin B) could be found in upper airway and be differentially regulated by different cytokines. SCGB3A2 (UGRP1) mRNA expression was induced by Th1 cytokine, but suppressed by proinflammatory and Th2 cytokines. SCGBs mRNA expression was altered in CRS; particularly, SCGB3A2 (UGRP1) protein and mRNA expression was markedly decreased in both CRSsNP and CRSwNP and its protein levels inversely correlated with the number of total infiltrating cells, preoperative sinonasal CT scores, and postoperative endoscopy and symptom scores. Conclusion SCGBs except SCGB1D2 (lipophilin B) are expressed in human upper airway and their expression can be differentially regulated by inflammatory cytokines. SCGBs mRNA expression is altered in CRS. Reduced production of UGRP1, which is likely due, at least in part, to a local cytokine environment, may contribute to the hyper-inflammation in CRS and correlates with response to surgery.

..., and their potential involvement, particularly that of SCGB3A2 (UGRP1), in chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP). Methods Eight SCGB family members including SCGB3A2 (UGRP1), SCGB1C1 (ligand binding protein RYD5), SCGB1D1 (lipophilin A), SCGB1D2 (lipophilin B), SCGB1D4 (interferon- inducible SCGB), SCGB2A1 (mammaglobin 2), SCGB2A2 (mammaglobin 1), and SCGB3A1 (uteroglobin-related protein 2) were studied. The regulation of SCGBs mRNA expression in

... rapidly expanding with the discovery of many new human genes. At present, nine members of this superfamily have been identified in humans, which includes SCGB1A1 (Clara cell 10-kDa protein, CC10), SCGB1C1 (ligand binding protein RYD5, RYD5), SCGB1D1 (lipophilin A, LIPA), SCGB1D2 (lipophilin B, LIPB), SCGB1D4 (interferon- inducible SCGB, IIS), SCGB2A1 (mammaglobin 2, MGB2), SCGB2A2 (mammaglobin 1, MGB1), SCGB3A1 (uteroglobin-related protein 2, UGRP2), and SCGB3A2 (uteroglobin-related protein 1, UGRP1

...- promoted, SCGB3A2 (UGRP1) mRNA expression in normal nasal mucosa. On the contrary, IL-1, TNF-, IL-4, and IL-13 enhanced, whereas IFN- suppressed, SCGB2A1 (MGB2) mRNA expression. Regarding SCGB1C1 (RYD5), IFN- down-regulated and IL-4 and IL-13 up-regulated its expression; however, no significant effect was observed for IL-1 and TNF-. Nevertheless, as to SCGB1D4 (IIS), IL-1, TNF-, and IFN- increased, but IL-4 and IL-13 decreased, its expression. With reference to SCGB1D1 (LIPA), its expression could be

... increase in CRSwNP. The expression of SCGB1C1 (RYD5) was only increased, whereas the expression of SCGB3A1 (UGRP2) was only decreased, in CRSwNP, and there was a significant difference between CRSsNP and CRSwNP. As to SCGB1D1 (LIPA), its expression was only enhanced in CRSsNP in comparison with control. We did not detect the SCGB1D2 (LIPB) mRNA expression in CRS either. Since the sample size of atopic or asthmatic patients was not large enough in either CRSsNP or CRSwNP group, we did not compare the

... (UGRP1) was also mainly produced by epithelial cells. By contrast, SCGB1C1 (RYD5) and SCGB1D4 (IIS) have, to the present author's knowledge, not been demonstrated in human respiratory airway mucosa until now, although SCGB1C1 (RYD5) and SCGB1D4 (IIS) have been detected in Bowman's glands of rat olfactory mucosa and human lymphoid tissues and cells, respectively [ 3 , 21 ]. The cellular locations of SCGB1C1 (RYD5) and SCGB1D4 (IIS) in sinonasal mucosa are unclear. Due to the lack of commercially

... cytokines. On the other hand, the same cytokine could evoke distinct responses of different SCGB genes. Our results suggest that the expression of SCGBs is finely controlled by local immune responses in airways and SCGBs may be involved in cytokine-induced airway inflammation. In present study, we found altered expression profiles of SCGBs in CRS. Since the biological functions of SCGBs are poorly understood, their roles in CRS mostly remain speculative. The unique increase of SCGB1C1 (RYD5) and

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Gene: SCGB1C1 - secretoglobin, family 1C, member 1 - (NCBI)

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