title: Coinfection with Clonorchis sinensis modulates murine host response against Trichinella spiralis infection.
abstract: Concomitant infections of different species of parasites are common in the field. Infection with one parasite species likely triggers host responses that may influence the subsequent infection of another species and alter disease outcomes. So far, the majority of studies have focused on single species parasite infection, and the mechanisms of protection induced by the first parasite infection against the secondary infection remain poorly defined. In this study, we assess the impact of trematode Clonorchis sinensis infection on the course of another tissue nematode Trichinella spiralis challenge. We observed that mice with preexisting C. sinensis infection had lower worm burden of intestinal T. spiralis than those infected with T. spiralis alone; mice with preexisting C. sinensis also had severe enteric histopathological changes and higher counts of intestinal Paneth cells in responses to T. spiralis challenge. The mRNA levels of interleukin (IL)-4, IL-10, IL-13, and tumor necrosis factor (TNF)-α from the small intestine and spleen of the different groups were analyzed using quantitative real-time polymerase chain reaction. Compared with that in mice infected with T. spiralis alone, the mRNA expression of IL-13 was significantly increased in the small intestine tissues and IL-4, IL-13, and TNF-α were significantly increased in the spleen tissues in the dually infected mice. Our findings suggest that a "preexisting" trematode infection of C. sinensis is a factor which contributes to reducing the establishment of T. spiralis adult worms in the small intestine.
authors.affiliation: Department of Parasitology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Bo
authors.initials: B
authors.lastname: Huang
authors.forename: Shiguang
authors.initials: S
authors.lastname: Huang
authors.forename: Xinbing
authors.initials: X
authors.lastname: Yu
authors.forename: Yonglong
authors.initials: Y
authors.lastname: Li
authors.forename: Wenjian
authors.initials: W
authors.lastname: Song
authors.forename: Yongxiang
authors.initials: Y
authors.lastname: Li
authors.forename: Fangli
authors.initials: F
authors.lastname: Lu
mesh_terms: D000818:Animals; D000909:Antibodies, Helminth / Q000097:blood*; D003003:Clonorchiasis / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D003004:Clonorchis sinensis / Q000276:immunology / Q000502:physiology; D060085:Coinfection; D004386:Duodenum / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D004804:Eosinophils / Q000166:cytology / Q000276:immunology; D005260:Female; D020397:Goblet Cells / Q000166:cytology / Q000276:immunology; D007378:Interleukins / Q000235:genetics; D007413:Intestinal Mucosa / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000166:cytology / Q000276:immunology; D051379:Mice; D019879:Paneth Cells / Q000166:cytology / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000276:immunology / Q000469:parasitology; D017160:Trichinella spiralis / Q000276:immunology*; D014235:Trichinellosis / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D000909:Antibodies, Helminth; D007378:Interleukins; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha