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High expression of eosinophil chemoattractant ecalectin/galectin‐9 in drug‐induced liver injury
Author(s) -
Takahashi Yoshihisa,
Fukusato Toshio,
Kobayashi Yuko,
Akiyama Shuichi,
Tamatani Takuya,
Shiga Junji,
Mori Shigeo
Publication year - 2006
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2005.01189.x
Subject(s) - pathology , eosinophilia , eosinophil , immunohistochemistry , medicine , liver biopsy , biopsy , liver injury , infiltration (hvac) , s100a9 , antibody , immunology , inflammation , asthma , physics , thermodynamics
Backgound: Ecalectin/galectin‐9 (ECL/GL9) is an eosinophil chemoattractant isolated from T lymphocytes. Drug‐induced liver injury (DILI), often caused by an allergic mechanism, is occasionally accompanied by eosinophilic infiltration. In this study, we intended to determine whether DILI can induce augmentation of ECL/GL9 expression. Further, we investigated whether this augmentation is associated with tissue eosinophilia. Methods: We examined the expression of ECL/GL9 in biopsy specimens of DILI using the immunohistochemical technique. A rabbit anti‐ECL/GL9 antibody was produced by immunizing rabbits with synthetic peptide corresponding to a molecular epitope of ECL/GL9. Thereafter, immunohistochemical staining with the use of this antibody was performed on 16 DILI needle biopsy specimens, and on biopsy specimens of chronic viral hepatitis, liver cirrhosis, and normal liver tissues as controls. Results: In all cases of DILI specimens, but not in control liver specimens, a clear positive staining for ECL/GL9 was observed. Such positive staining was noted on Kupffer cells, fibroblasts, and histiocytes, but not on lymphocytes or hepatocytes. However, the intensity of immunolabeling did not correlate with the extent of eosinophile leukocyte infiltration. Conclusion: High expression of ECL/GL9 is suggested to be a specific finding of DILI. However, tissue eosinophilia in DILI cannot be explained by the augmentation of ECL/GL9 expression.