Wednesday, July 6, 2011

What's new for 'Trypanosomatids' in PubMed

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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 - 6 of 6

1. Parasit Vectors. 2011 Jul 4;4(1):126. [Epub ahead of print]

Colonization of Phlebotomus papatasi changes the effect of pre-immunization with saliva from lack of protection towards protection against experimental challenge with Leishmania major and saliva.

Ben Hadj Ahmed S, Kaabi B, Chelbi I, Cherni S, Derbali M, Laouini D, Zhioua E.

Abstract

ABSTRACT:

BACKGROUND:

Sand fly saliva has been postulated as a potential vaccine or as a vaccine component within multi component vaccine against leishmaniasis. It is important to note that these studies were performed using long-term colonized Phlebotomus papatasi. The effect of sand flies colonization on the outcome of Leishmania infection is reported.

RESULTS:

While pre-immunization of mice with salivary gland homogenate (SGH) of long-term colonized (F5 and beyond) female Phlebotomus papatasi induced protection against Leishmania major co-inoculated with the same type of SGH, pre-immunization of mice with SGH of recently colonized (F2 and F3) female P. papatasi did not confer protection against L. major co-inoculated with the same type of SGH. Our data showed for the first time that a shift from lack of protection to protection occurs at the fourth generation (F4) during the colonization process of P. papatasi.

CONCLUSION:

For the development of a sand fly saliva-based vaccine, inferences based on long-term colonized populations of sand flies should be treated with caution as colonization of P. papatasi appears to modulate the outcome of L. major infection from lack of protection to protection.

PMID:
21726438
[PubMed - as supplied by publisher]
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2. Clin Exp Immunol. 2011 Jul 4. doi: 10.1111/j.1365-2249.2011.04430.x. [Epub ahead of print]

CD4(+) T cells defined by their Vβ T cell receptor expression are associated with immunoregulatory profiles and lesion size in human leishmaniasis.

Keesen TS, Antonelli LR, Faria DR, Guimarães LH, Bacellar O, Carvalho EM, Dutra WO, Gollob KJ.

Source

Department of Biochemistry and Immunology, Federal University of Minas Gerais Institute for Education and Research, Santa Casa Hospital René Rachou Institute, FIOCRUZ Department of Morphology, Federal University of Minas Gerais, Belo Horizonte, MG Immunology Service, Hospital Edgard Santos, UFBA-Salvador, Brazil INCT-DT Center for Infections Disease Research, Biosciences Division, SRI International, Menlo Park, CA, USA.

Abstract

Leishmaniasis is caused by infection with the protozoan parasite, Leishmania, that parasitizes human cells, and the cellular immune response is essential for controlling infection. In order to measure the host T cell response to Leishmania infection, we have measured the expansion, activation state and functional potential of specific T cells as identified by their T cell receptor Vβ region expression. In a group of cutaneous leishmaniasis (CL) patients, we evaluated these characteristics in nine different T cell subpopulations as identified by their Vβ region expression, before and after specific Leishmania antigen stimulation. Our results show: (1) an increase in CD4(+) T cells expressing Vβ 5·2 and Vβ 24 in CL compared to controls; (2) a Leishmania antigen-induced increase in CD4(+) T cells expressing Vβ 5·2, 11, 12 and 17; (3) a profile of previous activation of CD4(+) Vβ 5·2-, 11- and 24-positive T cells, with higher expression of CD45RO, HLA-DR, interferon-γ, tumour necrosis factor-α and interleukin-10 compared to other Vβ-expressing subpopulations; (4) a positive correlation between higher frequencies of CD4(+) Vβ5·2(+) T cells and larger lesions; and (5) biased homing of CD4(+) T cells expressing Vβ 5·2 to the lesion site. Given that CL disease involves a level of pathology (ulcerated lesions) and is often followed by long-lived protection and cure, the identification of specific subpopulations active in this form of disease could allow for the discovery of immunodominant Leishmania antigens important for triggering efficient host responses against the parasite, or identify cell populations most involved in pathology.

© 2011 The Authors. Clinical and Experimental Immunology © 2011 British Society for Immunology.

PMID:
21726211
[PubMed - as supplied by publisher]
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3. Arch Iran Med. 2011 Jul;14(4):288-9.

Causes of hepatic granuloma: a 12-year single center experience from southern iran.

Geramizadeh B, Jahangiri R, Moradi E.

Source

Transplant Research Center, Pathology Department, Shiraz University of Medical Sciences, Shiraz, Iran.geramib@sums.ac.ir.

Abstract

BACKGROUND:

Hepatic granuloma is reported in 2 - 15% of liver biopsy specimens. It is relatively easy for the pathologist to diagnose, but sometimes arriving at a specific etiology is quite difficult. Until now, there are few published studies about the etiology of hepatic granuloma in Iran. In this study, we attempt to determine the causes of hepatic granuloma from one of the largest referral centers in this country.

METHODS:

In a retrospective study over 12 years, a hepatopathologist reviewed all liver biopsies with granuloma. The medical records, including clinical findings, autoantibodies, viral markers, imaging studies, drug histories, and all other specialized tests, such as molecular studies, were reviewed to reach a definite diagnosis.

RESULTS:

During 12 years, there were 72 cases diagnosed with liver granuloma. The most common cause of hepatic granuloma was infectious, with Mycobacterium tuberculosis (52.8%). The second most common cause was visceral leishmaniasis in 8.3% of biopsies. Other less common causes were fungal infections, visceral larva migrans, primary biliary cirrhosis, and hepatitis C, each in 4.2% of cases. Autoimmune hepatitis was diagnosed in 2.8% of patients. Lymphoma, drug induced, disseminated BCGitis, CMV infection, foreign body reaction and sarcoidosis, were each found in 1.4% of the liver biopsies. After all investigations, there were 12.5% idiopathic hepatic granulomas.

CONCLUSION:

According to this study, the most common cause of hepatic granuloma in Iran is tuberculosis. This finding is completely different from western countries and very similar to the results of countries such as Saudi Arabia.

PMID:
21726107
[PubMed - in process]
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4. Arch Iran Med. 2011 Jul;14(4):238-43.

Comparative histological and immunohistochemical changes of dry type cutaneous leishmaniasi s after administration of meglumine antimoniate, imiquimod or combination therapy.

Shamsi Meymandi S, Javadi A, Dabiri S, Shamsi Meymandi M, Nadji M.

Source

Dermatology Department, Afzalipour Medical School, Kerman University of Medical Science, Kerman, Iran.meymandi_s@hotmail.com.

Abstract

BACKGROUND:

This study compared histological and immunohistochemical changes of cutaneous leishmaniasis treated with meglumine antimoniate, imiquimod, and the combination of both therapies.  

METHODS:

Single blind clinicopathological studies of fifteen patients with old world cutaneous leishmaniasis in Kerman, Iran were included. A total of four patients received a combination of imiquimod (5% cream) and intra-lesional meglumine antimoniate weekly for four weeks. Monotherapy with imiquimod was given to seven patients and four patients were treated with meglumine antimoniate intralesionally. Histological confirmation was performed before and during therapy. Semi-quantitative histological parameters such as numbers of mixed inflammatory cells (cells/mm2) and percentages of Langerhans cells (CD1a+), T-cells (CD3+), B-cells (CD20+), and macrophages (CD68+) were calculated immunohistochemically in the dermis and adjacent epidermis.  

RESULTS:

Topical imiquimod significantly reduced mean histiocytic cellular aggregation size (P<0.05). Meglumine antimoniate reduced parasite load and infected activated histiocytes in the dermis (P<0.05). Meglumine antimoniate therapy decreased epidermal CD3+ lymphocytes but increased them in the dermis, within the granulomas (P<0.05). During topical application of imiquimod a depletion of CD1a+ dendritic cells in the epidermis (P<0.05) and slight predominance of dendritic cells in the dermis were observed. Combined therapy and imiquimod monotherapy decreased CD68+ macrophages in the dermis (P<0.05).  

CONCLUSION:

Meglumine antimoniate decreases parasite load with considerable effect on up-regulation of T-cells, which demonstrates that meglumine antimoniate works as parasitocidal and immunomodulator, which could be a first line of treatment. Imiquimod accentuates the host immune response and reduces granuloma size which could be effective immunomodulator for combination therapy. Monotherapy of imiquimod is less effective than the two other regimens in decreasing parasite load, inflammation and congestion at the inoculated site.

PMID:
21726098
[PubMed - in process]
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5. PLoS One. 2011 Mar 18;6(3):e18013.

Identification of contractile vacuole proteins in Trypanosoma cruzi.

Ulrich PN, Jimenez V, Park M, Martins VP, Atwood J 3rd, Moles K, Collins D, Rohloff P, Tarleton R, Moreno SN, Orlando R, Docampo R.

Source

Center for Tropical and Emerging Global Diseases and Department of Cellular Biology, University of Georgia, Athens, Georgia, United States of America.

Abstract

Contractile vacuole complexes are critical components of cell volume regulation and have been shown to have other functional roles in several free-living protists. However, very little is known about the functions of the contractile vacuole complex of the parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, other than a role in osmoregulation. Identification of the protein composition of these organelles is important for understanding their physiological roles. We applied a combined proteomic and bioinfomatic approach to identify proteins localized to the contractile vacuole. Proteomic analysis of a T. cruzi fraction enriched for contractile vacuoles and analyzed by one-dimensional gel electrophoresis and LC-MS/MS resulted in the addition of 109 newly detected proteins to the group of expressed proteins of epimastigotes. We also identified different peptides that map to at least 39 members of the dispersed gene family 1 (DGF-1) providing evidence that many members of this family are simultaneously expressed in epimastigotes. Of the proteins present in the fraction we selected several homologues with known localizations in contractile vacuoles of other organisms and others that we expected to be present in these vacuoles on the basis of their potential roles. We determined the localization of each by expression as GFP-fusion proteins or with specific antibodies. Six of these putative proteins (Rab11, Rab32, AP180, ATPase subunit B, VAMP1, and phosphate transporter) predominantly localized to the vacuole bladder. TcSNARE2.1, TcSNARE2.2, and calmodulin localized to the spongiome. Calmodulin was also cytosolic. Our results demonstrate the utility of combining subcellular fractionation, proteomic analysis, and bioinformatic approaches for localization of organellar proteins that are difficult to detect with whole cell methodologies. The CV localization of the proteins investigated revealed potential novel roles of these organelles in phosphate metabolism and provided information on the potential participation of adaptor protein complexes in their biogenesis.

PMCID: PMC3060929
Free PMC Article
PMID:
21437209
[PubMed - indexed for MEDLINE]
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6. Parasitology. 2011 Feb;138(2):201-8.

Activity of the enzyme adenosine deaminase in serum, erythrocytes and lymphocytes of rats infected with Trypanosoma evansi.

da Silva AS, Bellé LP, Bitencourt PE, Souza VC, Costa MM, Oliveira CB, Jaques JA, Leal DB, Moretto MB, Mazzanti CM, Lopes ST, Monteiro SG.

Source

Department of Microbiology and Parasitology, Universidade Federal de Santa Maria, Brazil. aleksandro_ss@yahoo.com.br

Erratum in

  • Parasitology. 2011 Feb;138(2):266.

Abstract

In Trypanosoma evansi infections changes in the haemogram are commonly observed, and the enzyme adenosine deaminase (ADA) plays an important role in the production and differentiation of blood cells. Thus, the aim of this study was to evaluate the activity of ADA in serum, erythrocytes and lymphocytes of rats infected with T. evansi compared to non-infected rats. Thirty adult rats were used, divided into 3 uniform groups. The animals in groups A and B were infected intraperitoneally with 2 x 10⁶ trypomastigotes/rat. Rodents from group C (control group), were not-infected. Blood collection was performed on days 4 and 20 post-infection (p.i.) in order to obtain acute and chronic infection stages of disease. The blood was used to assess the activity of ADA. In the blood, reduced haematocrit and increased lymphocytes were correlated with ADA activity in erythrocytes and lymphocytes. We observed reduction of ADA activity in serum and erythrocytes in rats infected with T. evansi compared to non-infected rats (P < 0.05). ADA activity in lymphocytes was decreased after 4 days, when the parasitaemia was high and increased after 20 days, when the number of circulating parasites was low. In conclusion, our results showed that the ADA activity was altered in serum, lymphocytes and erythrocytes of rats, concomitantly with haematological parameters, in experimental infection by T. evansi.

PMID:
20809996
[PubMed - indexed for MEDLINE]
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