Chemokine tear levels in primary Sjögren’s syndrome and their relationship with symptoms

Hernández-Molina, Gabriela; Ruiz-Quintero, Narlly; Lima, Guadalupe; Hernández‐Ramírez, Diego F.; Llorente-Chávez, Amaya; Saavedra‐González, Vanessa; Jiménez-Soto, Rodolfo; Llórente, Luis

doi:10.1007/s10792-022-02233-5

Cited by 9 publications

(6 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, through tissue immunohistochemistry, our study supports the significant involvement of T cells and monocytes in the pathogenesis of pSS, consistent with prior research [ 39 ] . Several studies, including ours, have reported increased levels of CXCL9, 10, and 11 in salivary gland lesions [ 21 , 40 , 41 ], with similar findings observed in other tissues where dryness symptoms can manifest in patients with pSS, including the cervix, vagina, and tear glands [ 42 , 43 ]. Additionally, there have been reports of increased expression levels of CXCL9/10/11 in the conjunctival epithelium of pSS patients with xerophthalmia [ 44 ].…”

Section: Discussionsupporting

confidence: 80%

Role of chemokines CXCL9, CXCL10, CXCL11, and CXCR3 in the serum and minor salivary gland tissues of patients with Sjögren’s syndrome

Kim,

Ahn,

Jung

et al. 2024

Clin Exp Med

View full text Add to dashboard Cite

This study aimed to investigate the serum and expression levels of C-X-C motif chemokine ligand 9 (CXCL9), CXCL10, CXCL11, and CXC receptor 3 (CXCR3) in minor salivary glands (MSGs) of patients with primary Sjögren’s syndrome (pSS), and to explore their correlations with clinical parameters. Serum samples from 49 patients diagnosed with pSS, 33 patients with rheumatoid arthritis (RA), and 30 healthy controls (HCs) were collected for measurements of CXCL9, CXCL10, CXCL11, and CXCR3. Additionally, CXCL levels in the MSG tissues were measured in 41 patients who underwent MSG biopsy. Correlations between CXCL and CXCL/CXCR levels in serum/MSG tissues and clinical factors/salivary scintigraphy parameters were analyzed. Serum CXCL11 and CXCR3 showed statistically significant differences among patients with pSS and RA and HCs (serum CXCL11, pSS:RA:HC = 235.6 ± 500.1 pg/mL:90.0 ± 200.3 pg/mL:45.9 ± 53.6 pg/mL; p = 0.041, serum CXCR3, pSS:RA:HC = 3.27 ± 1.32 ng/mL:3.29 ± 1.17 ng/mL:2.00 ± 1.12 ng/mL; p < 0.001). Serum CXCL10 showed a statistically significant difference between pSS (64.5 ± 54.2 pg/mL) and HCs (18.6 ± 18.1 pg/mL, p < 0.001), while serum CXCL9 did not exhibit a significant difference among the groups. Correlation analysis of clinical factors revealed that serum CXCL10 and CXCL11 levels positively correlated with erythrocyte sedimentation rate (r = 0.524, p < 0.001 and r = 0.707, p < 0.001, respectively), total protein (r = 0.375, p = 0.008 and r = 0.535, p < 0.001, respectively), globulin (r = 0.539, p < 0.001 and r = 0.639, p < 0.001, respectively), and European Alliance of Associations for Rheumatology SS Disease Activity Index (r = 0.305, p = 0.033 and r = 0.321, p = 0.025). Additionally, serum CXCL10 negatively correlated with the Schirmer test score (r = − 0.354, p = 0.05), while serum CXCL11 positively correlated with the biopsy focus score (r = 0.612, p = 0.02). In the MSG tissue, the percentage of infiltrating CXCL9-positive cells was highest (75.5%), followed by CXCL10 (29.1%) and CXCL11 (27.9%). In the correlation analysis, CXCL11-expressing cells were inversely related to the mean washout percentage on salivary gland scintigraphy (r = − 0.448, p = 0.007). Our study highlights distinct serum and tissue chemokine patterns in pSS, emphasizing CXCL9’s potential for early diagnosis. This suggests that CXCL10 and CXCL11 are indicators of disease progression, warranting further investigation into their roles in autoimmune disorders beyond pSS.

show abstract

Section: Discussionsupporting

confidence: 80%

Role of chemokines CXCL9, CXCL10, CXCL11, and CXCR3 in the serum and minor salivary gland tissues of patients with Sjögren’s syndrome

Kim,

Ahn,

Jung

et al. 2024

Clin Exp Med

View full text Add to dashboard Cite

show abstract

“…Therefore, genes involved in these pathways and responses could be used as potential clinical indicators for the early diagnosis of SS-ILD, including CD58, CD86, CTLA4, CXCL8, SIGLEC1, and STAT1. The involvement of these genes in host immune and in ammatory responses has been documented to be related to various diseases, especially SS [21][22][23]. We also identi ed that upregulation of MUC1 was the main characteristic of patients with SS-ILD.…”

Section: Discussionmentioning

confidence: 74%

Modified Sanliangsan improved Sjogren’s syndrome complicated with interstitial lung disease by suppressing serum MUC1 levels

Tan,

Lv,

Chen

et al. 2024

Preprint

View full text Add to dashboard Cite

Objectives To clarify if the mechanism of Sanliangsan in improving Sjogren’s syndrome complicated with interstitial lung disease (SS-ILD) involves MUC1 suppression, which is involved in SS-ILD pathogenesis. Methods Fifty-six patients were randomly divided into two groups receiving Sanliangsan prescription therapy and conventional therapy. In-depth transcriptome profiles collected and analyzed to identify candidate genes involved in SS pathogenesis. Clinical symptom scores, metabolic compositions, lung HRCT scores, and serum MUC1 levels were compared between the two groups before and after treatment. Metabolome analyzed the metabolic composition of serum with SS-ILD before and after SP treatment. Results Transcriptome results identified the involvement of abnormal expression of genes relevant to the immune system, inflammatory responses, and signaling pathways. MUC1 was involved in SS pathogenesis and could be used to diagnose SS-ILD early. The SP therapy improved SS-ILD more effectively than conventional therapy. Moreover, Sanliangsan prescription therapy reduced serum MUC1 levels and restored the abnormal metabolisms, improving the abnormal inflammatory and immune responses of patients. Eugenol directly interacted with MUC1, and suppressed related genes, and was the bioactive compound of SP. Conclusion Modified Sanliangsan can improve the clinical symptoms, signs, and lung function of patients; the mechanism may be due to eugenol and related to MUC1 regulation

show abstract

“…The involvement of these genes in host immune and inflammatory responses has been documented to be related to various diseases, especially SS. 28 − 30 We also identified that upregulation of MUC1 was the main characteristic of patients with SS-ILD. Thus, MUC1 can be used as a biomarker for patients with SS-ILD.…”

Section: Discussionmentioning

confidence: 78%

Modified Sanliangsan Improved Sjogren’s Syndrome Complicated with Interstitial Lung Disease by Suppressing Serum MUC1 Levels

Tan,

Lv,

Chen

et al. 2024

ACS Omega

View full text Add to dashboard Cite

Objectives: To clarify if the mechanism of Sanliangsan in improving Sjogren's syndrome complicated with interstitial lung disease (SS-ILD) involves MUC1 suppression, which is involved in SS-ILD pathogenesis. Methods: Fifty-six patients were randomly divided into two groups receiving Sanliangsan prescription (SP) therapy and conventional therapy (western medicine). In-depth transcriptome profiles from a large database of SS-ILD patients were collected and analyzed to identify candidate genes involved in SS pathogenesis. Clinical symptom scores, metabolic compositions, lung HRCT (high-resolution computed tomography) scores, and serum MUC1 levels were compared between the two groups before and after treatment. Network pharmacology, molecular docking, and ITC assays were performed to identify bioactive compounds of SP in improving SS. Metabolome analyzed the metabolic composition of serum associated with SS-ILD before and after SP treatment. Results: Transcriptome results identified the involvement of abnormal expression of genes relevant to the immune system, inflammatory responses, and signaling pathways. Numerous genes, including CD58, CD86, CTLA4, CXCL8, STAT1, and especially MUC1, were involved in SS pathogenesis and could be used to diagnose SS-ILD early. Both treatments improved the lung HRCT scores and clinical symptoms of SS-ILD. The SP therapy improved SS-ILD more effectively than conventional therapy. Moreover, Sanliangsan prescription therapy reduced serum MUC1 levels and restored the abnormal metabolisms, improving the abnormal inflammatory and immune responses of patients. Eugenol directly interacted with MUC1, suppressed related genes, and was the bioactive compound of SP. SP could partially restore the abnormal metabolisms associated with SS-ILD pathogenesis. Conclusion: Based on conventional Western medicine treatment, modified Sanliangsan can significantly improve the clinical symptoms, signs, and lung function of patients; the mechanism may be due to eugenol and related to MUC1 regulation.

show abstract

Chemokine tear levels in primary Sjögren’s syndrome and their relationship with symptoms

Cited by 9 publications

References 23 publications

Role of chemokines CXCL9, CXCL10, CXCL11, and CXCR3 in the serum and minor salivary gland tissues of patients with Sjögren’s syndrome

Role of chemokines CXCL9, CXCL10, CXCL11, and CXCR3 in the serum and minor salivary gland tissues of patients with Sjögren’s syndrome

Modified Sanliangsan improved Sjogren’s syndrome complicated with interstitial lung disease by suppressing serum MUC1 levels

Modified Sanliangsan Improved Sjogren’s Syndrome Complicated with Interstitial Lung Disease by Suppressing Serum MUC1 Levels

Contact Info

Product

Resources

About