<i>Listeria monocytogenes</i> Inoculation Protects Mice against Blood-Stage <i>Plasmodium yoelii</i> Infection

Abstract

Listeria monocytogenes (Lm) has been used as the adjuvant or vector for tumor and viral vaccine for its capability of eliciting all aspects of cell-mediated immunity including T cell activation and interferon-gamma (IFN-γ) production. These effector components play critical roles in the protection against Plasmodium infection in both human malaria and mouse models. Therefore, immune response induced by Lm infection may benefit the defense against malaria. To test this hypothesis, we employed blood-stage Plasmodium yoelii (PyL) infected mice and challenged them with Lm. C57BL/6 and BALB/c mice that are sensitive to PyL infection were used in experiments. These two strains are resistant and sensitive, respectively, to Lm infection. The outcomes of double infection with PyL and Lm and the changes of immune response were investigated. We found that live Lm inoculation inhibited PyL multiplication in both C57BL/6 and BALB/c mice. Lm inoculation increased production of IFN-γ, infiltration of CD11b-positive macrophages and generation of nitric oxide in the spleen of C57BL/6 mice at day 5 after parasite infection. Both CD4-and CD8-positive T cells contributed to IFN-γ production induced by Lm inoculation in PyL-infected mice. The protective effect of Lm against PyL infection depended on the viability of the bacteria. Live Lm, rather than heat-killed Lm, stimulated early IFN-γ production which provided essential cytokine environment for the development of Th1 response in PyL-infected mice. Our data show for the first time that Lm inoculation has protective effect against blood-stage murine malaria, which provides a new clue for enhancing antiPlasmodium immunity.

Co‐infection with Chikungunya virus alters trafficking of pathogenic CD 8 + T cells into the brain and prevents Plasmodium ‐induced neuropathology

“…Worms [Schistosoma sp (Hartgers & Yazdanbakhsh, 2006;Waknine-Grinberg et al, 2010;Bucher et al, 2011;Wang et al, 2013Wang et al, , 2014, Litomosoides sigmodontis (Karadjian et al, 2014), and Heligmosomoides polygyrus (Su et al, 2005)] and bacteria [Mycobacterium tuberculosis (Li & Zhou, 2013), Listeria monocytogenes (Qi et al, 2013), and Salmonella (Cunnington et al, 2012)] have been shown to alter the pathological outcome of malaria infection through bystander regulation of the host immunity. Specific to the PbA-ECM model, the mechanisms leading to ECM protection during co-infection were mostly due to the suppression of the pro-inflammatory response induced by the heterologous pathogen, which occurs from 4 days post-Plasmodium infection onwards.…”

Chlamydial Pre-Infection Protects from Subsequent Herpes Simplex Virus-2 Challenge in a Murine Vaginal Super-Infection Model

“…major footpad lesion development [ 40 ]. Prior infection with either Listeria monocytogenes or Mycobacterium tuberculosis can protect from subsequent lethal infection from Plasmodium yoelii [ 41 , 42 ]. In each instance, the establishment of protection against the secondary infection was attributed to the production of pro-inflammatory cytokines by the first pathogen [ 40 – 42 ].…”

Malaria-Cutaneous Leishmaniasis Co-infection: Influence on Disease Outcomes and Immune Response

“…Some cases of human Malaria and VL co-infection were described in the past and recently in different parts of the world ( Yoeli, 1948 ; Ab Rahman and Abdullah, 2011 ; van den Bogaart et al, 2012 , 2014 ; Bin Mohanna, 2015 ), demonstrating that co-infection may occur more frequently than we would expect. An increasing amount of evidence shows that co-infections may affect the natural outcome and progression of diseases due to the modulation of immune response ( La Flamme et al, 2002 ; Kolbaum et al, 2012 ; Qi et al, 2013 ; van den Bogaart et al, 2014 ). In the present study, we established a co-infection model of American CL and a non-lethal murine Malaria and demonstrated that co-infection is able to affect the pathogenesis and outcome of both diseases.…”