ABSTRACT
The spleen plays a crucial role in the development of immunity to malaria, but the role of pattern recognition receptors (PRRs) in splenic effector cells during malaria infection is poorly understood. In the present study, we analysed the expression of selected PRRs in splenic effector cells from BALB/c mice infected with the lethal and non-lethal Plasmodium yoelii strains 17XL and 17X, respectively, and the non-lethal Plasmodium chabaudi chabaudi AS strain. The results of these experiments showed fewer significant changes in the expression of PRRs in AS-infected mice than in 17X and 17XL-infected mice. Mannose receptor C type 2 (MRC2) expression increased with parasitemia, whereas Toll-like receptors and sialoadhesin (Sn) decreased in mice infected with P. chabaudi AS. In contrast, MRC type 1 (MRC1), MRC2 and EGF-like module containing mucin-like hormone receptor-like sequence 1 (F4/80) expression decreased with parasitemia in mice infected with 17X, whereas MRC1 an MRC2 increased and F4/80 decreased in mice infected with 17XL. Furthermore, macrophage receptor with collagenous structure and CD68 declined rapidly after initial parasitemia. SIGNR1 and Sn expression demonstrated minor variations in the spleens of mice infected with either strain. Notably, macrophage scavenger receptor (Msr1) and dendritic cell-associated C-type lectin 2 expression increased at both the transcript and protein levels in 17XL-infected mice with 50% parasitemia. Furthermore, the increased lethality of 17X infection in Msr1 -/- mice demonstrated a protective role for Msr1. Our results suggest a dual role for these receptors in parasite clearance and protection in 17X infection and lethality in 17XL infection.
Subject(s)
Animals , Female , Mice , Lectins, C-Type/immunology , Malaria/parasitology , Mannose-Binding Lectins/immunology , Plasmodium chabaudi/immunology , Plasmodium yoelii/immunology , Receptors, Cell Surface/immunology , Receptors, Scavenger/immunology , Spleen/parasitology , Toll-Like Receptors/immunology , Flow Cytometry , Lectins, C-Type/genetics , Mice, Inbred BALB C , Microarray Analysis , Malaria/immunology , Mannose-Binding Lectins/genetics , Parasitemia/immunology , Receptors, Cell Surface/genetics , Receptors, Scavenger/genetics , Spleen/immunology , Toll-Like Receptors/geneticsABSTRACT
OBJECTIVE: To evaluate the capacity of Lactobacillus casei ssp. rhamnosus to enhance resistance against Plasmodium chabaudi chabaudi AS. MATERIAL AND METHODS: NIH mice were IP injected with viable lactobacillus casei seven days (LC1 group) or 7 and 14 days (LC2 group) before the challenge (day 0) with Plasmodium chabaudi parasitized red blood cells (pRBC). Control mice were inoculated with pRBC only. When parasitaemia was resolved, naive mice were injected with spleen cells from each group. The parasitaemia was measured. Nitric oxide (NO.) in serum was determined. RESULTS: Mice from the LC1 group presented a reduction in parasitaemia, with a prepatent period of five days, parasitaemia lasted 11 days, and the peak was (36.3 percent pRBC) on the 12th day post-infection. Mice from the LC2 group showed a prepatent period of five days, parasitaemia lasted eight days, and the peak (30 percent pRBC) was of on the 11th day. In the control, the prepatent period was three days, the parasitaemia lasted 15 days, and the peak (51 percent pRBC) was on day nine. Mice inoculated with spleen cells from the LC2 group showed a prepatent period of 21 days, parasitaemia lasted seven days, and the peak (13.5 percent pRBC) was on the 26th day. CONCLUSION: L. casei enhanced nonspecific resistance to P. chabaudi, as indicated by longer prepatent periods, reduced parasitaemia, and reduction in the viability of the parasites recovered from the spleen of infected mice, along with high concentrations of NO. in serum.
OBJETIVO: Evaluar la capacidad de Lactobacillus casei de aumentar la resistencia a la infección con Plasmodium chabaudi en ratones. MATERIAL Y MÉTODOS: Ratones NIH fueron inyectados intraperitonealmente con L. casei viable 7 días (grupo LC1) o 7 y 14 días (grupo LC2) antes del reto (día 0) con glóbulos rojos parasitados (GRP) con P. chabaudi. Los testigos fueron inoculados con GRP solamente. Cuando la parasitemia se resolvió, se inocularon ratones limpios con células de bazo de cada grupo. Se midió la concentración de óxido nítrico (NO.) en suero. RESULTADOS: El grupo LC1 presentó un periodo prepatente de 5 días, una parasitemia de 11 días con el máximo (36.3 por ciento de GRP) el día 12. Los ratones del grupo LC2 mostraron un periodo prepatente de 5 días, una parasitemia de 8 días con el pico (30 por ciento de GRI) el día 11. En los testigos el periodo prepatente fue de 3 días, la parasitemia de 15 y su máximo (51 por ciento de GRI) el día 9. Los ratones que recibieron células de bazo del grupo LC2, mostraron un período prepatente de 21 días, una parasitemia de 7 con su máximo (13.5 por ciento de GRI) el día 26. CONCLUSION: L. casei aumenta la resistencia no específica hacia P. chabaudi a juzgar por los periodos prepatentes más largos, las bajas parasitemias, la reducción en la viabilidad y la elevación de la concentración de NO. en el suero, que presentaron los ratones estimulados con lactobacilos.
Subject(s)
Animals , Mice , Lacticaseibacillus casei/immunology , Malaria/immunology , Plasmodium chabaudi/immunology , Probiotics , Erythrocytes/parasitology , Immunity, Innate , Malaria/blood , Malaria/parasitology , Nitric Oxide/blood , Parasitemia/diagnosis , Plasmodium chabaudi/isolation & purification , Spleen/cytology , Spleen/immunology , Time FactorsABSTRACT
This work aimed to study the T helper type 1/2 (Th1/Th2) cytokine profile in a co-infection murine model of Plasmodium chabaudi chabaudi and Leishmania infantum. Expression of interferon-gamma and interleukin-4 (IL-4) was analyzed, in spleen and liver of C57BL/6 mice, by reverse transcriptase-polymerase chain reaction. High levels of IFN-gamma expression did not prevent the progression of Leishmania in co-infected mice and Leishmania infection did not interfere with the Th1/Th2 switch necessary for Plasmodium control. The presence of IL-4 at day 28 in co-infected mice, essential for Plasmodium elimination, was probably a key factor on the exacerbation of the Leishmania infection.