Excretory/secretory products from Trichinella spiralis adult worms ameliorate DSS-induced colitis in mice.
BACKGROUND
Many evidences show the inverse correlation between helminth infection and allergic or autoimmune diseases. Identification and characterization of the active helminth-derived products responsible for the beneficial effects on allergic or inflammatory diseases will provide another feasible approach to treat these diseases.


RESULTS
Colitis was induced in C57BL/6 mice by giving 3% DSS orally for 7 days. During this period, the mice were treated daily with the excretory/secretory products from T. spiralis adult worms (AES) intraperitoneally. The severity of colitis was monitored by measuring body weight, stool consistency or bleeding, colon length and inflammation. To determine the T. spiralis AES product-induced immunological response, Th1, Th2, Th17 and regulatory cytokine profiles were measured in lymphocytes isolated from colon, mesenteric lymph nodes (MLN), and the spleen of treated mice. The CD4+ CD25+ FOXP3+ regulatory T cells (Tregs) were also measured in the spleens and MLN of treated mice. Mice treated with AES significantly ameliorated the severity of the DSS-induced colitis indicated by the reduced disease manifestations, improved macroscopic and microscopic inflammation correlated with the up-regulation of Treg response (increased regulatory cytokines IL-10, TGF-beta and regulatory T cells) and down-regulation of pro-inflammatory cytokines (IFN-gamma, IL-6 and IL-17) in the spleens, MLN and colon of treated mice.


CONCLUSIONS
Our results provide direct evidences that T. spiralis AES have a therapeutic potential for alleviating inflammatory colitis in mice. This effect is possibly mediated by the immunomodulation of regulatory T cells to produce regulatory and anti-inflammatory cytokines and inhibit pro-inflammatory cytokines.
Department of Parasitology, School of Basic Medical Sciences, Capital Medical University, Beijing, China; Department of Microbiology and Parasitology, Bengbu Medical College; Anhui Key Laboratory of Infection and Immunity, Bengbu, Anhui, China.
Xiaodi
X
Yang
Department of Parasitology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yaping
Y
Yang
Department of Parasitology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yunyun
Y
Wang
Section of Tropical Medicine, Department of Pediatrics, Baylor College of Medicine, Houston, Texas, United States of America.
Bin
B
Zhan
Department of Parasitology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yuan
Y
Gu
Department of Parasitology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Yuli
Y
Cheng
Department of Parasitology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Xinping
X
Zhu
D000818:Animals; D001688:Biological Products / Q000008:administration & dosage / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D003092:Colitis / Q000139:chemically induced / Q000517:prevention & control*; D003106:Colon / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D016264:Dextran Sulfate; D003967:Diarrhea / Q000517:prevention & control; D005260:Female; D005434:Flow Cytometry; D051858:Forkhead Transcription Factors / Q000378:metabolism; D007274:Injections, Intraperitoneal; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D008198:Lymph Nodes / Q000187:drug effects / Q000378:metabolism; D008214:Lymphocytes / Q000187:drug effects / Q000378:metabolism; D008810:Mice, Inbred C57BL; D013154:Spleen / Q000187:drug effects / Q000378:metabolism; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000378:metabolism; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000378:metabolism; D016896:Treatment Outcome; D017160:Trichinella spiralis / Q000737:chemistry*
D001688:Biological Products; D016207:Cytokines; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D053645:Interleukin-2 Receptor alpha Subunit; D016264:Dextran Sulfate