Stimulation of TH1 Response by Helicobacter Pylori Neutrophil Activating Protein Decreases the Protective Role of IgE and Eosinophils in Experimental Trichinellosis
Free accessResearch articleFirst published online October, 2011
Stimulation of TH1 Response by Helicobacter Pylori Neutrophil Activating Protein Decreases the Protective Role of IgE and Eosinophils in Experimental Trichinellosis
Th2 responses seem to play an important role in defence against Trichinella spiralis (Ts). The Neutrophil Activating Protein of Helicobacter pylori (HP-NAP), that induces IL-12, and IL-23 expression and shifts to Th1 allergen-specific Th2 cells in vitro was used as an anti-Th2 agent in BALB/c mice infected with T. spiralis. The muscle larvae (ML) burden was lower (p < 0.02) in untreated infected animals than those infected treated with HP-NAP. In both groups there was an inverse relationship between ML burden of each animal and total IgE level (controls: r −0.617, p = 0.0013 and HP-NAP-treated: r −0.678, P = 0.0001) or eosinophil count, evaluated in the same mouse on day 42 (r −0.390, P = 0.0592 and r −0.803, P = 0.0001, respectively). Inflammatory response around the nurse cell-parasite complex was significantly higher in HP-NAP-treated infected animals than in those untreated infected, on the contrary the number of eosinophils, counted around each complex was significantly lower in the first animal group. This study provides evidence of a powerful anti-Th2 activity in vivo by HP-NAP and for the partial protective effect of Th2 responses in T. spiralis infection.
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