Wednesday, April 8, 2009

What's new for 'Trypanosomatids' in PubMed

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Sent on Wednesday, 2009 Apr 08
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: Am J Pathol. 2009 Apr 6. [Epub ahead of print]

Altered Dendritic Cell Phenotype in Response to Leishmania amazonensis Amastigote Infection Is Mediated by MAP Kinase, ERK.

Boggiatto PM, Jie F, Ghosh M, Gibson-Corley KN, Ramer-Tait AE, Jones DE, Petersen CA.

From the Immunobiology Program,* Department of Veterinary Pathology, and Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine Iowa State University, Ames, Iowa; and the Lois Pope LIFE Center, University of Miami Leonard M. Miller School of Medicine, Miami, Florida.

Initiation of productive immune responses against Leishmania depends on the successful transition of dendritic cells (DC) from an immature to a mature phenotype. This process is characterized by high CD40 surface expression as well as interleukin-12 production, which are frequently seen in response to L. major infection. In vivo footpad infection of C3HeB/FeJ mice for 7 days with L. amazonensis promoted an immature CD11c(+) DC phenotype characterized by both significantly low CD40 surface expression and significantly decreased interleukin-12p40 production compared with L. major infection of these same mice. In vitro infection of bone marrow-derived dendritic cells with L. amazonensis amastigotes resulted in rapid and significant phosphorylation of the mitogen activated protein kinase, extracellular signal-regulated kinase 1/2, observed within minutes of exposure to the parasite. Infection with L. amazonensis promastigotes led to increased 1/2 phosphorylation after 4 hours of infection compared with L. major infection, which correlated with promastigote transformation into amastigotes. Treatment of bone marrow-derived dendritic cells with a mitogen activated protein kinase kinase-specific inhibitor, PD98059, led to regained surface CD40 expression and interleukin-12p40 production following L. amazonensis amastigote infection compared with non-treated, infected DC. Treatment of L. amazonensis-infected mice with the highly-specific mitogen activated protein kinase kinase inhibitor, CI-1040, enhanced surface CD40 expression on CD11c(+) DC obtained from the draining lymph node. L. amazonensis amastigotes, through activation of extracellular signal-regulated kinase 1/2, inhibit the ability of DC to undergo proper maturation both in vitro and in vivo.

PMID: 19349356 [PubMed - as supplied by publisher]

2: J Dermatol. 2009 Apr;36(4):209-12.

Evaluation of insulin resistance in obese women with and without acanthosis nigricans.

Sadeghian G, Ziaie H, Amini M, Ali Nilfroushzadeh M.

Skin Disease and Leishmaniasis Research Center, Isfahan, Iran. Sadeghian@sdlrc.mui.ac.ir

Acanthosis nigricans is characterized by hyperpigmented velvety plaques of body folds and neck. Insulin could be a responsible factor in the pathogenesis of this condition and hyperinsulinemia: a consequence of insulin resistance stimulates the formation of these characteristic plaques. In this study, insulin resistance was compared in obese women with and without acanthosis nigricans. This was a cross-sectional study. Sixty-six obese women (32 patients with acanthosis nigricans and 34 patients without acanthosis nigricans) were selected randomly. Levels of fasting serum insulin and fasting blood glucose were measured in both groups and insulin resistance was determined using homeostasis model assessment. Glucose tolerance test also was performed for all of participants. Five (15.6%) patients with acanthosis nigricans and no (0%) patient without acanthosis nigricans had insulin resistance (P < 0.05). Six (18.7%) patients with acanthosis nigricans and one (2.9%) patient without acanthosis nigricans had impaired glucose tolerance test (P < 0.05). The mean levels of fasting serum insulin were 15.7 +/- 8.7 and 12.2 +/- 4.1 microm/mL (P < 0.05) and the mean values of insulin resistance index were 3.5 +/- 1.9 and 2.6 +/- 0.9 microm/mL between patients with and without acanthosis nigricans, respectively (P < 0.05). In Iranian obese women, acanthosis nigricans is a marker of insulin resistance.

PMID: 19348659 [PubMed - in process]

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