Increased susceptibility to Strongyloides venezuelensis infection is related to the parasite load and absence of major histocompatibility complex (MHC) class II molecules

Abstract

In human and murine models strongyloidiasis induce a Th2 type response. In the current study we investigated the role of different loads of Strongyloides venezuelensis in the immune response raised against the parasite and the participation of the major histocompatibility complex (MHC) class II molecule in the disease outcome in face of the different parasite burden. The C57BL/6 wild type (WT) and MHC II(-/-) mice were individually inoculated by subcutaneous injection with 500 or 3000 S. venezuelensis L3. The MHC II(-/-) mice infected with 3000L3 were more susceptible to S. venezuelensis infection when compared with WT groups, in which the parasite was completely eliminated. The production of Th2 cytokines and specific IgG1 or IgE antibodies against parasite were significantly lowered in MHC II(-/-) infected mice with different larvae inoculums. The infection of MHC II(-/-) mice with S. venezuelensis induced slight inflammatory alterations in the small intestine, and these lesions were lower when compared with WT mice, irrespective of the parasite load utilized to infect animals. Finally, we concluded that MHC class II molecules are essential in the immune response against S. venezuelensis mainly when infection occurs with high parasite inoculum.

Differences in the Importance of Mast Cells, Basophils, IgE, and IgG versus That of CD4+T Cells and ILC2 Cells in Primary and Secondary Immunity to Strongyloides venezuelensis

“…We found that T and B cell-deficient Rag2 -/-mice exhibited a 20-day delay (i.e., requiring 32 days in total) in cessation of S. venezuelensis egg excretion during primary infections and a 25-day delay (i.e., requiring 37 days in total) in the secondary infection (versus no eggs detected during secondary infections in any of the wild-type mice) (Fig. 3A), underscoring the importance of an adaptive immune response for effective secondary immune responses to this nematode (8,11,13,14,41,(46)(47)(48). In addition, we confirmed that the number of adult worms in the intestines on day 8 of the primary infection was significantly higher in the Rag2 -/-mice than in the corresponding wild-type mice (Fig.…”

Inducible nitric oxide synthase controls experimental Strongyloides infection

“…The interaction between Strongyloides sp. and the host is generally characterized by the T helper type 2 response (Th2), with consequent cytokine production, eosinophilia and production of antibodies . Although the role of NO in infection by Strongyloides sp.…”

“…and the host is generally characterized by the T helper type 2 response (Th2), with consequent cytokine production, eosinophilia and production of antibodies. 9,14 Although the role of NO in infection by Strongyloides sp. is still unknown, there are reports in the literature showing that molecules usually related to the Th1 profile, such as NO, can contribute to the elimination of or resistance to infection by extracellular parasites, such as Giardia lamblia, 34 Entamoeba histolytica, 35 Brugia malayi, 36 Taenia crassiceps 37 and Schistosoma mansoni.…”

“…venezuelensis infects wild rats and has been used in experimental models to understand the effector responses as well as the immunoregulatory or immunoprotective reactions raised by the host, similarly to the events observed in S . stercoralis infection in humans . Among the various effector immune mechanisms described in helminth infections, the role of nitric oxide (NO) has also been reported .…”

“…reactions raised by the host, similarly to the events observed in S. stercoralis infection in humans. 9,10 Among the various effector immune mechanisms described in helminth infections, the role of nitric oxide (NO) has also been reported. [11][12][13][14][15] Production of NO is often associated with activation of macrophages by IFNγ and increased microbicidal mechanisms against intracellular pathogens such as Leishmania sp., Trypanosoma cruzi, Toxoplasma gondii and Plasmodium sp.…”