title: The absence of MyD88 has no effect on the induction of alternatively activated macrophage during Fasciola hepatica infection.
abstract: Alternatively activated macrophages (AAMφ) play important roles in allergies and responses toparasitic infections. However, whether signaling through toll-like receptors (TLRs) plays any role in AAMφ induction when young Fasciola hepatica penetrates the liver capsule and migrates through the liver tissue is still unclear.
  
  
  RESULTS
  The data show that the lack of myeloid differentiation factor 88 (MyD88) has no effect on the AAMφ derived from the bone marrow (BMMφ) in vitro and does not impair the mRNA expression of arginase-1, resistin-like molecule (RELMα), and Ym1 in BMMφs. The Th2 cytokine production bias in splenocytes was not significantly altered in F. hepatica-infected mice in the absence of MyD88 in vitro and in the pleural cavity lavage in vivo. In addition, MyD88-deficiency has no effect on the arginase production of the F. hepatica elicited macrophages (Fe Mφs), production of RELMα and Ym1 proteins and mRNA expression of Ym1 and RELMα of macrophages in the peritoneal cavity 6 weeks post F. hepatica infection.
  
  
  CONCLUSIONS
  The absence of MyD88 has no effect on presence of AAMφ 6 weeks post F. hepatica infection.
authors.affiliation: Laboratory of Infection & Immunology Research, College of Animal Science & Technology, Southwest University, Chongqing, China. lhl200296@yahoo.cn
authors.forename: HongLin
authors.initials: H
authors.lastname: Luo
authors.forename: Weiyi
authors.initials: W
authors.lastname: Huang
authors.forename: Dongying
authors.initials: D
authors.lastname: Wang
authors.forename: Haoju
authors.initials: H
authors.lastname: Wang
authors.forename: Kui
authors.initials: K
authors.lastname: Nie
mesh_terms: D000818:Animals; D001119:Arginase / Q000378:metabolism; D002478:Cells, Cultured; D003170:Complement Pathway, Alternative; D016207:Cytokines / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D005210:Fasciola hepatica / Q000276:immunology; D005211:Fascioliasis / Q000235:genetics / Q000276:immunology*; D005786:Gene Expression Regulation / Q000235:genetics / Q000276:immunology; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D037102:Lectins / Q000235:genetics / Q000378:metabolism; D008099:Liver / Q000473:pathology*; D008262:Macrophage Activation / Q000235:genetics; D008264:Macrophages / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D058408:Th1-Th2 Balance; D001619:beta-N-Acetylhexosaminidases / Q000235:genetics / Q000378:metabolism
chemical_list: D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D037102:Lectins; D053594:Myeloid Differentiation Factor 88; C413576:Retnla protein, mouse; C429541:Chil3 protein, mouse; D001619:beta-N-Acetylhexosaminidases; D001119:Arginase
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