The online version of this article (doi:10.1186/1475-2875-11-104) contains supplementary material, which is available to authorized users.
The authors declare that they have no competing interests.
WYX designed research; YF, YD, TLZ, XLF performed research; WYX analysed data and wrote paper. All authors have read and approved the final manuscript.
Toll-like receptors (TLRs) signalling is reported to be primed by the infection of human malaria parasite, Plasmodium falciparum. However, little is known about the regulation of macrophages TLR signalling by the infection of lethal or non-lethal strain of rodent malaria parasites.
BALB/c mice were infected with non-lethal strain Plasmodium yoelii 17XNL or lethal strain P. yoelii 17XL. Peritoneal macrophages were isolated to study its immune response to pRBC lysate, and TLRs (TLR2, TLR4, and TLR9) agonists, and the expression of TLRs and intracellular signalling molecules were also investigated by flow cytometry and semi-quantitive RT-PCR.
The reactivity of peritoneal macrophages from the mice infected with lethal strain P. y 17XL or non-lethal strain P. y 17XNL were enhanced to pRBC lysate, and TLR2, TLR4, and TLR9 agonists at one, three and five days post-infection. Of all the tested TLRs, only TLR2 was up-regulated on peritoneal macrophages of mice infected with either strain. However, transcription of intracellular signalling molecules MyD88, IRAK-1, and TRAF-6 was significantly up-regulated in peritoneal macrophages from mice infected either with P. yoelii 17XL or P. yoelii 17XNL at one, three and five days post-infection. However, the enhanced TLRs response of macrophage from P. yoelii 17XNL-infected mice persisted for a much longer time than that from P. yoelii 17XL-infected mice.
Both P. yoelii 17XL and 17XNL strains could enhance the response of peritoneal macrophages to pRBC lysate and TLR agonists, through up-regulating the expression of TLR2 and intracellular signalling molecules MyD88, IRAK-1, and TRAF-6. In addition, prolonged high response of macrophage from P. yoelii 17XNL-infected mice might be associated with the more efficiently controlling of P. yoelii 17XNL growth in mice at early stage.
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WHO: World Malaria Report. 2009, [ http://www.who.int/malaria/world_malaria_report_2009/en/index.html]
Mohan K, Moulin P, Stevenson MM: Natural killer cell cytokine production, not cytotoxicity, contributes to resistance against blood-stage Plasmodium chabaudi AS infection. J Immunol. 1997, 159: 4990-4998. PubMed
Freitas do Rosario AP, Voisine C, Mastelic B, Thompson J, Koernig S, Jarra W, Renia L, Mauduit M, Potocnik AJ, Langhorne J, Sponaas AM: Migrating monocytes recruited to the spleen play an important role in control of blood stage malaria. Blood. 2009, 114: 5522-5531. 10.1182/blood-2009-04-217489. CrossRefPubMed
Zhu J, Krishnegowda G, Gowda DC: Induction of proinflammatory responses in macrophages by the glycosylphosphatidylinositols of Plasmodium falciparum: the requirement of extracellular signal-regulated kinase, p38, c-Jun N-terminal kinase and NF-kappaB pathways for the expression of proinflammatory cytokines and nitric oxide. J Biol Chem. 2005, 280: 8617-8627. CrossRefPubMed
Krishnegowda G, Hajjar AM, Zhu J, Douglass EJ, Uematsu S, Akira S, Woods AS, Gowda DC: Induction of proinflammatory responses in macrophages by the glycosylphosphatidylinositols of Plasmodium falciparum: cell signaling receptors, glycosylphosphatidylinositol (GPI) structural requirement, and regulation of GPI activity. J Biol Chem. 2005, 280: 8606-8616. CrossRefPubMed
Parroche P, Lauw FN, Goutagny N, Latz E, Monks BG, Visintin A, Halmen KA, Lamphier M, Olivier M, Bartholomeu DC, Gazzinelli RT, Golenbock DT: Malaria hemozoin is immunologically inert but radically enhances innate responses by presenting malaria DNA to Toll-like receptor 9. Proc Natl Acad Sci USA. 2007, 104: 1919-1924. 10.1073/pnas.0608745104. PubMedCentralCrossRefPubMed
Nomura F, Akashi S, Sakao Y, Sato S, Kawai T, Matsumoto M, Nakanishi K, Kimoto M, Miyake K, Takeda K, Akira S: Cutting edge: endotoxin tolerance in mouse peritoneal macrophages correlates with down-regulation of surface toll-like receptor 4 expression. J Immunol. 2000, 164: 3476-3479. CrossRefPubMed
Franklin BS, Parroche P, Ataíde MA, Lauw F, Ropert C, de Oliveira RB, Pereira D, Tada MS, Nogueira P, da Silva LH, Bjorkbacka H, Golenbock DT, Gazzinelli RT: Malaria primes the innate immune response due to interferon-gamma induced enhancement of toll-like receptor expression and function. Proc Natl Acad Sci USA. 2009, 106: 5789-5794. 10.1073/pnas.0809742106. PubMedCentralCrossRefPubMed
Hartgers FC, Obeng BB, Voskamp A, Larbi IA, Amoah AS, Luty AJ, Boakye D, Yazdanbakhsh M: Enhanced Toll-like receptor responsiveness associated with mitogen-activated protein kinase activation in Plasmodium falciparum-infected children. Infect Immun. 2008, 76: 5149-5157. 10.1128/IAI.01579-07. PubMedCentralCrossRefPubMed
Landau I, Chabaud AG: Natural infection by 2 plasmodia of the rodent Thamnomys rutilans in the Central African Republic. Comptes Rendus Hebdomadaires des Seances de l' Academie des Sciences. D: Sciences Naturelles. 1965, 261: 230-232.
Yoeli M, Hargreaves B, Carter R, Walliker D: Sudden increase in virulence in a strain of Plasmodium berghei yoelii. Ann Trop Med Parasitol. 1975, 69: 173-178. PubMed
Otsuki H, Kaneko O, Thongkukiatkul A, Tachibana M, Iriko H, Takeo S, Tsuboi T, Torii M: Single amino acid substitution in Plasmodium yoelii erythrocyte ligand determines its localization and controls parasite virulence. Proc Natl Acad Sci USA. 2009, 106: 7167-7172. 10.1073/pnas.0811313106. PubMedCentralCrossRefPubMed
- Plasmodium yoelii blood-stage primes macrophage-mediated innate immune response through modulation of toll-like receptor signalling
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