China Journal of Leprosy and Skin Diseases ›› 2024, Vol. 40 ›› Issue (6): 406-411.doi: 10.12144/zgmfskin202406406

• Original Articles • Previous Articles     Next Articles

Expression of SlC35E family in leprosy lesions

XU Zongyan1*, LI Yang2*, LIN Xiuqiu2, LIN Junjie2, WANG Xiaohua2   

  1. 1 Futian Center For Chronic Disease Control, Shenzhen 518000, China; 2 Department of Dermatology, Dermatology Hospital, Southern Medical University, Guangzhou 510091, China
    * Co-first author
  • Online:2024-06-15 Published:2024-05-07

Abstract: Objective: To determine the difference of solute transporter family protein SLC35E between multibacillary and paucibacterial leprosy lesions. Methods: First, paraffin-embedded skin tissues of 25 patients with leprosy were collected, including 12 of multibacillary leprosy and 13 of  paucibacillary leprosy. The mutations of different SNPS of SLC35E1 and SLC35E2B were analyzed. At the same time, skin tissues of 12 healthy controls were collected as normal control group. Immunohistochemical staining was used to detect the expression differences of SLC35E1, SLC35E2B, CD68 and S100 in the above lesions and normal control group. Immunofluorescence staining was used to detect the co-expression of CD68 and S100 with SLC35E1 and SLC35E2B proteins in skin lesions. Results: Bioinformatics analysis of 25 leprosy tissue samples showed that the mutation rate of SNP rs202071873 of SLC35E1 in leprosy patients was 0%. SLC35E2B three SNPS loci rs12729295, rs117820608, rs2072923 mutation rate in leprosy patients were 100%, 40%, 100%. Immunohistochemical staining showed that SLC35E1, SLC35E2B, CD68 and S100 were expressed in the dermis and epidermis of leprosy tissues, among which CD68 was mainly expressed in the dermis of leprosy tissues, and the expression of SLC35E1 in the dermis was basically consistent with that of CD68, and there was a positive correlation between them. There was no significant difference in the expression of S100 between epidermis and dermis of leprosy patients, and no significant correlation with the expression of SLC35E1 and SLC35E2B. Compared with paucibacillary leprosy patients, SLC35E1 of multibacillary leprosy patients in the dermis was lower expression (P=0.046). Compared with healthy controls, the SLC35E2B of multibacillary leprosy patients in the epidermal layer was lower expression (P=0.004). Immunofluorescence co-staining showed that CD68 overlapped with SLC35E1 and SLC35E2B proteins in leprosy lesions, and the overlap fluorescence intensity with SLC35E1 was higher than that with SLC35E2B. No overlapping results were observed when S100 was co-stained with SLC35E1 and SLC35E2B proteins. Conclusion: There may be mutations in the SLC35E2B locus in leprosy lesions of  patients, and the expression of SLC35E1 may predict the difference between MB and PB infection in dermis. SLC35E1 and SLC35E2B may interfere with the clearance of M. leprae by affecting the function of macrophages, thereby affecting the pathogenesis of leprosy.

Key words: immune response, macrophages, leprosy, SLC35E1, SLC35E2B, CD68, S100