, 2002, Lawrence, 2003 and Wynn, 2003). In similar conditions, primarily infected Bos taurus cattle and sheep ( Claerebout et al., 2005 and Lacroux et al., 2006), as well as resistant Nellore cattle ( Zaros et al., 2010), had high levels of these cytokines. TNF-α is a pro-inflammatory factor that may have an important Sunitinib order role in gastrointestinal infections. Hayes et al. (2007) observed that TNF-α acts to increase both cytokines Th1 (IFN-γ) and Th2 (IL-13). Although this pattern is not

well established yet, functions related to Th2 polarization have been reported (Artis et al., 1999). Some works concluded that this pro-inflammatory factor is associated to resistance in sheep (Pernthaner et al., 2005) and cattle (Li et al., 2007). In our work, Dasatinib TNF-α was about eight

times higher in the lymph node (Fig. 2) and fourfold less expressed in the abomasal mucosa (Fig. 3) of the infected animals compared to the uninfected ones. A contrasting pattern was observed in both tissues studied. The presence of TNF-α was characterized to potentialize the expulsion of parasites by IL-13, conferring protection in the host (Artis et al., 1999), as well as, it was correlated to induction of host resistance in early larval stages (Babu and Nutman, 2004). So, differences of TNF-α found in the two tissues studied could be a result of tissue collection when the immune response started to be established and when changes in larval stages were still ongoing. Then, although, at this time, this cytokine could be helping the Th2

polarization in the lymph nodes, the presence of parasitic secretions in the abomasum could exert some local immunomodulation. It is known that the Haemonchus spp. L4 larvae stage is capable of inducing changes in the host immune profile to evade host response ( Allen and MacDonald, 1998). As in early infection stages, TNF-α has been reported to promote parasite expulsion, this molecule could be a target for immunomodulation by the parasite ( Maizels and Yazdanbakhsh, 2003). TNF-α down-regulation may be caused by mast cell inhibition Cytidine deaminase and may turn resistant animals in susceptible ( Behnke et al., 2003 and Pernthaner et al., 2005). Therefore, maintaining low TNF-α level in the host would be beneficial for completion of parasitic life cycle. Artis et al. (1999) found that low TNF-α level delays the expulsion of parasites from the host and that IL-4 and IL-13 levels remain up-regulated, as observed in this work. During gastrointestinal infections, increases of mast cells and eosinophils are usually observed (Gasbarre, 1997 and Else, 2005). In sheep, these cells are involved in rejection of H. contortus. Eosinophils are recruited to the abomasum of sheep during primary infection ( Balic et al., 2000 and Balic et al., 2002) and are related to death of the parasite ( Balic et al., 2006).