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Highly up‐regulated CXCR3 expression on eosinophils in mice infected with Schistosoma japonicum
Author(s) -
Li He,
Chunsong Hu,
Guobin Cai,
Qiuping Zhang,
Qun Li,
Xiaolian Zhang,
Baojun Huang,
Linjie Zhang,
Junyan Liu,
Mingshen Jiang,
Jinquan Tan
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2004.01771.x
Subject(s) - schistosoma japonicum , cxcl10 , cxcr3 , biology , chemokine , chemokine receptor , ccr3 , cxcl9 , immunology , ccr2 , microbiology and biotechnology , inflammation , schistosomiasis , helminths
Summary CXCR3, predominately expressed on memory/activated T cells, is a receptor for both interferon‐γ inducible protein‐10/CXC ligand 10 (CXCL10) and monokine induced by interferon‐γ/CXCL9. We reported here that CXCR3 was highly up‐regulated on infiltrating eosinophils in Schistosoma japonicum egg‐induced granuloma in the mouse liver. It was also highly and functionally up‐regulated on peritoneal exudate eosinophils in mice infected with S. japonicum. The phenomena were demonstrated at protein and mRNA levels using immunohisto‐ and immunocytochemistry evaluation of biopsy, flow cytometry and real‐time quantitative reverse transcriptase–polymerase chain reaction technique, and verified by Northern blotting and chemotaxis assay in vitro . We also found that CCR3 expression on the infiltrating and peritoneal exudate cells was significantly decreased, CXCR4 expression was unchanged during the 42‐day period of infection. We screened mRNA expression levels of the all known chemokine receptors in purified peritoneal exudate eosinophils and liver granuloma dominated by eosinophils. CXCR3 was highly and functionally up‐regulated on peritoneal exudate eosinophils in mice infected with S. japonicum, meanwhile CCR3 was significantly and functionally down‐regulated in these cells. The findings could lead to a better understanding of the chemokine receptor expression pattern of eosinophils at inflamed tissue sites caused by parasites. These could be also crucial for establishing a therapeutic strategy for eosinophilic inflammation via intervention in chemokine actions.