What's new for 'Trypanosomatids' in PubMed

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Sent on Tuesday, 2010 Aug 17
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 - 2 of 2

1.	J Eukaryot Microbiol. 2010 Aug 5. [Epub ahead of print] Evidence for Rosettes as an Unrecognized Stage in the Life Cycle of Leishmania Parasites. Iovannisci DM, Paul Plested C, Moe GR. Center for Immunobiology and Vaccine Development, Children's Hospital and Research Center Oakland, 5700 Martin Luther King Jr. Way, Oakland, California 94609. Abstract Leishmania parasites, which afflict 12 million people in 88 countries, exist as promastigotes transmitted by insect vectors and as amastigotes residing in mammalian macrophages. Promastigote cells arranged in rosettes have also been described but universally disregarded as a distinct stage in the life cycle. We present evidence that only rosettes of Leishmania major promastigotes express cell surface poly-alpha2,8 N-acetyl neuraminic acid (PSA) and PSA containing de-N-acetyl neuraminic acid (NeuPSA). Expression of rosette-specific PSA antigens was mosaic, with individual promastigotes expressing PSA, NeuPSA or both. A 50 kDa protein was detected by Western blot analysis of a detergent-insoluble cell fraction with both PSA and NeuPSA-reactive antibodies. Frequencies of rosette formation as well as cell surface PSA/NeuPSA expression were temperature dependent. Rosettes also engaged in an unusual swarming behavior, congregating into extended clusters. Distinct structures resembling cellular fusion bodies were formed in and released from rosettes. The results indicate that rosettes are an unrecognized stage in the life cycle of Leishmania. We hypothesize that rosettes initiate mating in Leishmania during which PSA/NeuPSA expression plays an important role. Recognizing rosettes as a distinct form of the Leishmania life cycle opens new possibilities for treatment or prevention of disease and, possibly, in vitro genetic recombination without passage of cells through insect vectors.
	PMID: 20707828 [PubMed - as supplied by publisher]
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2.	Exp Dermatol. 2010 Aug 12. [Epub ahead of print] Human primary dendritic cell subsets differ in their IL-12 release in response to Leishmania major infection. Zahn S, Kirschsiefen P, Jonuleit H, Steinbrink K, von Stebut E. Department of Dermatology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. Abstract Immunity against leishmaniasis has primarily been studied in experimental infections of mice. It was shown that infected skin dendritic cells (DC) are critical for the induction of protection against this pathogen, and targeting skin DC in vaccination approaches in mice has proven to be successful. However, little is known about the contribution of human DC subsets from the skin to primary immunity against this pathogen. In this study, we have analysed the interaction between different human DC subsets and Leishmania major. Primary human myeloid and monocyte-derived DC ingested the parasite comparable to that of murine skin DC, and this resulted in DC activation and IL-12 release, a cytokine essential for the induction of Th1/Tc1-dependent protection. Interestingly, both Langerhans cells and plasmacytoid DC did not appear to contribute to protection in humans. Thus, in leishmaniasis, both murine and human data suggest that dermal inflammatory DC appear to be superior in promoting protection.
	PMID: 20707811 [PubMed - as supplied by publisher]
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