Expression of non-TLR pattern recognition receptors in the spleen of BALB/c mice infected with Plasmodium yoelii and Plasmodium chabaudi chabaudi AS.

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.

[1]  J. A. Mabel,et al.  Hyperphagia induced by ventricular pressure and pentobarbitone in normal and hypothalmic obese rats. , 1966, Lancet.

[2]  L. Weiss,et al.  Mechanisms of splenic control of murine malaria: reticular cell activation and the development of a blood-spleen barrier. , 1986, The American journal of anatomy.

[3]  M. Hommel,et al.  Plasmodium chabaudi: a rodent malaria model for in‐vivo and in‐vitro cytoadherence of malaria parasites in the absence of knobs , 1987, Parasite immunology.

[4]  J. Langhorne,et al.  Limiting dilution analysis of the T cell response to Plasmodium chabaudi chabaudi in mice , 1989, Parasite immunology.

[5]  L. Weiss.  Mechanisms of splenic control of murine malaria: cellular reactions of the spleen in lethal (strain 17XL) Plasmodium yoelii malaria in BALB/c mice, and the consequences of pre-infective splenectomy. , 1989, The American journal of tropical medicine and hygiene.

[6]  F. Hackett,et al.  Signal transduction in host cells by a glycosylphosphatidylinositol toxin of malaria parasites , 1993, The Journal of experimental medicine.

[7]  P. Gerold,et al.  Glycosylphosphatidylinositol toxin of Plasmodium induces nitric oxide synthase expression in macrophages and vascular endothelial cells by a protein tyrosine kinase-dependent and protein kinase C-dependent signaling pathway. , 1996, Journal of immunology.

[8]  A. Richards.  Tumour necrosis factor and associated cytokines in the host's response to malaria. , 1997, International journal for parasitology.

[9]  T. Kodama,et al.  Involvement of macrophage scavenger receptors in protection against murine malaria. , 1998, The American journal of tropical medicine and hygiene.

[10]  Catherine E. Costello,et al.  Glycosylphosphatidylinositol anchors of Plasmodium falciparum: molecular characterization and naturally elicited antibody response that may provide immunity to malaria pathogenesis. , 2000 .

[11]  K. Kain,et al.  Nonopsonic monocyte/macrophage phagocytosis of Plasmodium falciparum-parasitized erythrocytes: a role for CD36 in malarial clearance. , 2000, Blood.

[12]  D. Gowda,et al.  Plasmodium falciparumGlycosylphosphatidylinositol-induced TNF-α Secretion by Macrophages Is Mediated without Membrane Insertion or Endocytosis* , 2001, The Journal of Biological Chemistry.

[13]  K. Kain,et al.  Mechanism of protection induced by vitamin A in falciparum malaria , 2002, The Lancet.

[14]  Salvatore Musumeci,et al.  The immune response to Plasmodium falciparum malaria. , 2002, The Lancet. Infectious diseases.

[15]  E. Riley,et al.  Innate immunity to malaria , 2004, Nature Reviews Immunology.

[16]  Lynette Beattie,et al.  The importance of the spleen in malaria. , 2005, Trends in parasitology.

[17]  L. Schofield,et al.  Immunological processes in malaria pathogenesis , 2005, Nature Reviews Immunology.

[18]  S. Akira,et al.  Induction of Proinflammatory Responses in Macrophages by the Glycosylphosphatidylinositols of Plasmodium falciparum , 2005, Journal of Biological Chemistry.

[19]  B. Urban,et al.  Early interactions between blood-stage plasmodium parasites and the immune system. , 2005, Current topics in microbiology and immunology.

[20]  S Gordon,et al.  Macrophage receptors and immune recognition. , 2005, Annual review of immunology.

[21]  D. Ferguson,et al.  Fatal Plasmodium falciparum Malaria Causes Specific Patterns of Splenic Architectural Disorganization , 2005, Infection and Immunity.

[22]  Siamon Gordon,et al.  The carbohydrate-recognition domain of Dectin-2 is a C-type lectin with specificity for high mannose. , 2006, Glycobiology.

[23]  Hiroshi Suzuki,et al.  Short report: role of type I/II scavenger receptors in malarial infection in C57BL/6J mice. , 2006, The American journal of tropical medicine and hygiene.

[24]  I. Clark,et al.  Human malarial disease: a consequence of inflammatory cytokine release , 2006, Malaria Journal.

[25]  Hiroshi Suzuki,et al.  ROLE OF TYPE I/II SCAVENGER RECEPTORS IN MALARIAL INFECTION IN C57BL/6J MICE , 2006 .

[26]  D. Underhill,et al.  Dectin-2 Is a Pattern Recognition Receptor for Fungi That Couples with the Fc Receptor γ Chain to Induce Innate Immune Responses* , 2006, Journal of Biological Chemistry.

[27]  Infection by and protective immune responses against Plasmodium berghei ANKA are not affected in macrophage scavenger receptors A deficient mice , 2006, BMC Microbiology.

[28]  Samir N. Patel,et al.  Disruption of CD36 Impairs Cytokine Response to Plasmodium falciparum Glycosylphosphatidylinositol and Confers Susceptibility to Severe and Fatal Malaria In Vivo1 , 2007, The Journal of Immunology.

[29]  K. Kain,et al.  Inflammatory pathways in malaria infection: TLRs share the stage with other components of innate immunity. , 2008, Molecular and biochemical parasitology.

[30]  P. Taylor,et al.  Dectin-2 is a Syk-coupled pattern recognition receptor crucial for Th17 responses to fungal infection , 2009, The Journal of experimental medicine.

[31]  S. Grinstein,et al.  CD36 and TLR Interactions in Inflammation and Phagocytosis: Implications for Malaria1 , 2009, The Journal of Immunology.

[32]  S. Gordon,et al.  Scavenger receptors: role in innate immunity and microbial pathogenesis , 2009, Cellular microbiology.

[33]  G. Milon,et al.  Retention of erythrocytes in the spleen: a double-edged process in human malaria , 2009, Current opinion in hematology.

[34]  D. Gowda,et al.  Proinflammatory responses by glycosylphosphatidylinositols (GPIs) of Plasmodium falciparum are mainly mediated through the recognition of TLR2/TLR1. , 2011, Experimental parasitology.

[35]  J. Ordi,et al.  Strain-specific spleen remodelling in Plasmodium yoelii infections in Balb/c mice facilitates adherence and spleen macrophage-clearance escape , 2011, Cellular microbiology.

[36]  T. Abo,et al.  Cytokine profile of murine malaria: stage-related production of inflammatory and anti-inflammatory cytokines. , 2011, Biomedical research.