The absence of MyD88 has no effect on the induction of alternatively activated macrophage during Fasciola hepatica infection

The data show that the lack of myeloid differentiation factor 88 (MyD88) has no effect on the AAM？ derived from the bone marrow (BMM？) in vitro and does not impair the mRNA expression of arginase-1, resistin-like molecule (RELMα), and Ym1 in BMM？s. 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 M？s), 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.The absence of MyD88 has no effect on presence of AAM？ 6 weeks post F. hepatica infection.Macrophages are highly plastic cells that respond to diverse environments by altering their phenotype and physiology [1,2] and play important roles in both innate and adaptive immunity. Currently, macrophages are classified under two phenotypes, classically activated macrophages (CAMΦ) and alternatively activated macrophages (AAMΦ). CAMΦ are induced by interferon-gamma (IFN-γ) and lipopolysaccharide (LPS), whereas induction of the AAMΦ phenotype is associated with various stimuli, such as IL-4/IL-13, IL-10, immunocomplexes, and glucocorticoids [2]. The most widely studied stimuli for generating AAMΦ is treatment with IL-4/IL-13 [1,3]. Although IL-4/IL-13 signaling are essential to the presence of AAMΦ and both cytokines have many overlapping activities on macrophages, they exhibit distinct functions because of their specific receptor subunits aside from their shared common alpha chain [4]. However, this does not alter the fact that a Th2-dominated environment is critical for AAMΦ induction [5-7]. All helminths have been demonstrated to induce profound Th2 responses, which are characterized by the production of IL-4, IL-5, IL-9, IL-10, and IL-13 by CD4+ T cells [8], and this Th2-dominated cy