What's new for 'Trypanosomatids' in PubMed

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Sent on Thursday, 2011 Oct 20
Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results

Items 1 - 4 of 4

1.	MBio. 2011 Oct 18;2(5). pii: e00226-11. doi: 10.1128/mBio.00226-11. Print 2011. The Coxiella burnetii Dot/Icm System Creates a Comfortable Home through Lysosomal Renovation. Newton HJ, Roy CR. Source Section of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut, USA. Abstract ABSTRACT Understanding the molecular pathogenesis of Coxiella burnetii, the causative agent of human Q fever, has historically been hindered by the technical difficulties of genetically manipulating obligate intracellular bacteria. The recent development of culture conditions suitable for axenic propagation of C. burnetii has paved the way for the application of a range of genetic techniques to address key questions within the field. Recent studies using mutational analysis have revealed that the C. burnetii Dot/Icm type 4 secretion system (T4SS) is an important virulence determinant that is essential for renovation of a lysosome into a mature Coxiella-containing vacuole (CCV) permissive of intracellular replication. Interestingly, a mutant of C. burnetii deficient in Dot/Icm function was found to be capable of replicating within the parasitophorous vacuole created by Leishmania amazonensis, which indicates that C. burnetii replication is not dependent on the cohort of Dot/Icm effector proteins per se but rather that the collective actions of effectors are required to create the specialized niche supportive of replication. Thus, a role for the Dot/Icm T4SS during the intracellular life cycle of C. burnetii has been more clearly defined by these studies, which demonstrate that advances in genetic analysis should allow future studies to focus on the intricacies of Dot/Icm effector functions that facilitate development of the unique CCV.
	PMID: 22010216 [PubMed - in process]

2.	N Engl J Med. 2011 Sep 29;365(13):1258-9; author reply 1259. Antitrypanosomal therapy for chronic Chagas' disease. Bestetti RB, Cardinalli-Neto A. Comment on N Engl J Med. 2011 Jun 30;364(26):2527-34.
	PMID: 21991909 [PubMed - indexed for MEDLINE]
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3.	N Engl J Med. 2011 Sep 29;365(13):1258; author reply 1259. Antitrypanosomal therapy for chronic Chagas' disease. Garcia-Bournissen F, Altcheh J. Comment on N Engl J Med. 2011 Jun 30;364(26):2527-34.
	PMID: 21991908 [PubMed - indexed for MEDLINE]
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4.	J Immunol. 2011 Sep 1;187(5):2656-65. Epub 2011 Jul 29. Myeloid-derived suppressor cells infiltrate the heart in acute Trypanosoma cruzi infection. Cuervo H, Guerrero NA, Carbajosa S, Beschin A, De Baetselier P, Gironès N, Fresno M. Source Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Cantoblanco, 28049 Madrid, Spain. Abstract Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, affects several million people in Latin America. Myocarditis, observed in the acute and chronic phases of the disease, is characterized by a mononuclear cell inflammatory infiltrate. We previously identified a myeloid cell population in the inflammatory heart infiltrate of infected mice that expressed arginase I. In this study, we purified CD11b(+) myeloid cells from the heart and analyzed their phenotype and function. Those CD11b(+) cells were ∼70% Ly6G(-)Ly6C(+) and 25% Ly6G(+)Ly6C(+). Moreover, purified CD11b(+)Ly6G(-) cells, but not Ly6G(+) cells, showed a predominant monocytic phenotype, expressed arginase I and inducible NO synthase, and suppressed anti-CD3/anti-CD28 Ab-induced T cell proliferation in vitro by an NO-dependent mechanism, activity that best defines myeloid-derived suppressor cells (MDSCs). Contrarily, CD11b(+)Ly6G(+) cells, but not CD11b(+)Ly6G(-) cells, expressed S100A8 and S100A9, proteins known to promote recruitment and differentiation of MDSCs. Together, our results suggest that inducible NO synthase/arginase I-expressing CD11b(+)Ly6G(-) myeloid cells in the hearts of T. cruzi-infected mice are MDSCs. Finally, we found plasma l-arginine depletion in the acute phase of infection that was coincident in time with the appearance of MDSCs, suggesting that in vivo arginase I could be contributing to l-arginine depletion and systemic immunosuppression. Notably, l-arginine supplementation decreased heart tissue parasite load, suggesting that sustained arginase expression through the acute infection is detrimental for the host. This is, to our knowledge, the first time that MDSCs have been found in the heart in the context of myocarditis and also in infection by T. cruzi.
	PMID: 21804013 [PubMed - indexed for MEDLINE]
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