Recombinant Brugia malayi pepsin inhibitor (rBm33) induced monocyte function and absence of apoptotic cell death: An in vitro study

Sreenivas, Kirthika; Vijayan, Kamalakannan; Babu, Subash; Narayanan, R. B.

doi:10.1016/j.micpath.2012.03.009

Cited by 4 publications

(2 citation statements)

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“…It consists of roughly 85% alpha-helix, and its binding to the human pepsin indicates a 1:1 complex formation [ 38 ]. Recombinant rBm33 has been shown to stimulate macrophages to produce a Th1 response but did not induce apoptosis [ 39 ]. Immunolocalization of the native protein defined a widespread distribution, both on the surface of the parasite and in internal organs [ 40 ].…”

Section: Recombinant Antigensmentioning

confidence: 99%

Recombinant antigens used as diagnostic tools for lymphatic filariasis

et al. 2021

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Lymphatic filariasis (LF) is a parasitic disease caused by the worms Wuchereria bancrofti, Brugia malayi, or Brugia timori. It is a tropical and subtropical illness that affects approximately 67 million people worldwide and that still requires better diagnostic tools to prevent its spread and enhance the effectiveness of control procedures. Traditional parasitological tests and diagnostic methods based on whole protein extracts from different worms are known for problems related to sample time collection, sensitivity, and specificity. More recently, new diagnostic tools based on immunological methods using recombinant antigens have been developed. The current review describes the several recombinant antigens used as tools for lymphatic filariasis diagnosis in antigen and antibody capture assays, highlighting their advantages and limitations as well as the main commercial tests developed based on them. The literature chronology is from 1991 to 2021. First, it describes the historical background related to the identification of relevant antigens and the generation of the recombinant polypeptides used for the LF diagnosis, also detailing features specific to each antigen. The subsequent section then discusses the use of those proteins to develop antigen and antibody capture tests to detect LF. So far, studies focusing on antibody capture assays are based on 13 different antigens with at least six commercially available tests, with five proteins further used for the development of antigen capture tests. Five antigens explored in this paper belong to the SXP/RAL-2 family (BmSXP, Bm14, WbSXP-1, Wb14, WbL), and the others are BmShp-1, Bm33, BmR1, BmVAH, WbVAH, BmALT-1, BmALT-2, and Wb123. It is expected that advances in research with these antigens will allow further development of tests combining both sensitivity and specificity with low costs, assisting the Global Program to Eliminate Lymphatic Filariasis (GPELF).

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Section: Recombinant Antigensmentioning

confidence: 99%

Recombinant antigens used as diagnostic tools for lymphatic filariasis

et al. 2021

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“…Few in vitro studies on this gene are currently available. Studies on apoptosis of individual peripheral blood monocytes showed that the reduced IL-10 expression in RBM33 stimulated the major Th1 response in THP-1 monocytes, which was antigen-specific, but RBM33 did not induce apoptosis of either monocytes or lymphocytes ( 36 ). We also found that RBM33 did not affect apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Epigenome-Wide Association Study Reveals Differential Methylation Sites and Association of Gene Expression Regulation with Ischemic Moyamoya Disease in Adults

Duan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. The association of DNA methylation with the pathogenesis of adult ischemic moyamoya disease (MMD) is unknown. Here, we investigated the genome-wide DNA methylation profiles in patients with MMD and identified the genes related to the pathogenesis of MMD. Methods. Whole blood samples were collected from 20 individuals, including 10 patients with ischemic moyamoya disease without any underlying disease and 10 healthy individuals. Genome-wide DNA methylation analysis was performed using Illumina 850K microarrays. Transcriptional correlation was verified using quantitative reverse transcription-polymerase chain reaction. In vitro experiments were used to analyze the association of functional defects with candidate epigenetic markers. Results. The genome-wide methylation level in the whole blood of adults with ischemic MMD was higher than that in the healthy individuals. In total, 759 methylation probes differed significantly between the case and control. The hypermethylated regions were mostly concentrated in the gene spacer regions. Among genes with the highest degree of the differential expression, KCNMA1 and GALNT2 were upregulated, whereas SOX6 and RBM33 were downregulated. Conclusions. This is the first study showing that the low expression of genes associated with epigenetic regulation, such as SOX6 and RBM33, may be related to vascular occlusion in MMD, whereas the overexpression of KCNMA1 and GALNT2 may be related to the vascular hyperplasia. The results suggest that DNA methylation was involved in the pathogenesis of MMD, and new pathogenic genes were proposed as biological markers.

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