Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA384259 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5481730_1.fastq.gz | Fastqsanger.gz | |||
| SRR5481730_2.fastq.gz | Fastqsanger.gz | |||
| SRR5481740_1.fastq.gz | Fastqsanger.gz | |||
| SRR5481740_2.fastq.gz | Fastqsanger.gz | |||
| SRR5481750_1.fastq.gz | Fastqsanger.gz |
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Project description:The debilitating disease kala-azar or visceral leishmaniasis (VL) is caused by the kinetoplastid protozoan parasite Leishmania donovani. The parasite is transmitted by the hematophagous sandfly vector of the genus Phlebotomus in the old world and Lutzomyia in the new world. The predominant Phlebotomine species associated with transmission of kala-azar are Phlebotomus papatasi and Phlebotomus argentipes. The infected female sandfly transmits the parasite when it takes a blood meal. Understanding the molecular interaction of the sand fly-Leishmania during the development of parasite within the gut of the sandfly is crucial to understanding parasite life cycle. The complete genome sequences of sandfly vectors (Phlebotomus and Lutzomyia) are currently not available and sequencing efforts are underway. Non-availability of genome sequence can hamper identification of proteins in the sandfly vector. In the present study we have carried out proteogenomic analysis of unsequenced sandfly vector P. paptasi cell line using high-resolution mass spectrometry and comparative homology-based searches using related dipteran protein data (mosquitoes and fruit fly). This study resulted in identification of 1,312 proteins from P. papatasi based on homology. Our study demonstrates the power of proteogenomic approaches in mapping the proteomes of unsequenced organisms.
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Project description:Visceral leishmaniasis (VL) in Sudan caused by Leishmania donovani is fatal in susceptible individuals if untreated. Treatment with Sodium Stibogluconate (SSG) leads to post kala azar dermal leishmaniasis (PKDL) in 58% of patients. Here Affymetrix microarrays were used to identify genes differentially expressed in lymph nodes (N=9 paired samples) pre- and post-treatment with SSG. Using the Bioconductor package limma, 438 genes from 28,869 post quality-control probe-sets were differentially expressed (Pnominal≤0.02) post- versus pre-treatment. Canonical pathway analysis using Ingenuity Pathway Analysis identified “Role of NFAT in Regulation of Immune Response” (Pnominal=1.35x10-5; PBH-adjusted=4.79x10-3), “B Cell Development” (Pnominal=2.04x10-4; PBH-adjusted=0.024), “Fcγ Receptor-mediated Phagocytosis in Macrophages and Monocytes” (Pnominal=2.04x10-4; PBH-adjusted=0.024), and “OX40 Signaling” (Pnominal=2.82x10-4; PBH-adjusted=0.025) as pathways differentially regulated post- versus pre-treatment. Major network hub genes included TP53, FN1, MYC, BCL2, JUN, SYK, RUNX2, MMP1 and ACTA2. Top endogenous upstream regulators included IL-7 (P=2.28x10-6), TNF (P=4.26x10-6), APP (P=4.23x10-5) and SPI1/PI.1 (P=1.17x10-7). Top predicted chemical drug regulators included the flavonoid genistein (P=4.56x10-7) and the quinoline alkaloid camptothecin (P=5.14x10-5). These results contribute to our understanding of immuno-pathology associated with VL and response to SSG treatment. Further replication could identify novel therapeutic strategies that improve on SSG treatment and reduce the likelihood of progression to PKDL.
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Project description:Post Kala Azar Dermal Leishmaniasis (PKDL) is a non-fatal dermal sequel of Visceral Leishmaniasis (VL), caused by protozoan parasite Leishmania donovani. On the global scenario, PKDL in mainly restricted to distinct zones of South Asia (India, Nepal and Bangladesh) and East Africa, mainly Sudan. In India, the most prominent fatal form of leishmaniasis present is VL, affecting entirely the eastern region of the country. The clinical presentation of VL and PKDL differ substantially; where VL patients suffer from sustained fever, hepatospleenomegaly, weight loss and anemia, PKDL patients manifest dermal lesions in the form of macular, nodular and polymorphic. Although, compared to VL, the mortality rate of PKDL is significantly lower, yet it is observed as a stigmatizing disease that brings a substantial socioeconomic burden, further intensified by a hesitancy of patients, to obtain treatment, or due to noncompliance. Lesions, especially the polymorphic forms, are parasite-rich, concluding that PKDL plays a crucial role in the anthroponotic transmission of VL. PKDL patients with Macular lesions, having comparatively lower parasitic load, and thus lacks detection sensitivity with standard techniques like rK39 (73% sensitivity), Leishmanin skin test (54% sensitivity) and Histopathological studies with patients’ skin biopsy sample (7-33% sensitivity) and is often misdiagnosed as Vitiligo cases. In order to completely eliminate Kala-azar in Southeast Asia, proper identification of various routes of the disease is essential, which could efficiently distinguish between cured PKDL and active PKDL as well as active PKDL from other cross disease like Leprosy and Vitiligo. Till now very less work has been done towards biomarker identification for PKDL from patients’ plasma. Most of the methods for disease identification are based on highly invasive tissue biopsy followed by PCR/qPCR. Recently investigations from our group have demonstrated the presence of novel glycoproteins in the circulating immune complexes (CICs) from serum, as biomarkers for early identification of PKDL patients. An Immune complex (IC), sometimes called an antigen-antibody complex, is a molecule formed from the integral binding of an antibody to a soluble antigen. After an antigen-antibody reaction, the immune complexes can be subject to any number of responses, including complement deposition, opsonisation, phagocytosis, or processing by proteases. Accumulation of ICs leads to a broad spectrum of pro-inflammatory effects, including activation of the complement cascade and induction of cytokine secretion. These complexes may also be deposited in tissues and vessel walls, leading to inflammation, tissue damage and, ultimately, disease manifestations. Immune complexes also affect disease progression and outcome in various disorders through the induction of pro-inflammatory or anti-inflammatory cytokines. In the present study we hypothesize that the CICs’ proteome is altered among PKDL patients with different dermal manifestations (Macular and Polymorphic) as compared to Cured individuals (CR) and Healthy controls (HI). The aim of this current study is to identify differentially expressed CIC proteomic profile among different forms PKDL patients as compared to HI. The differential protein expression of specific unique peptide fragments, representing specific proteins, could be used as diagnostic biomarkers in early detection of both Macular and Polymorphic PKDL cases. In this prospective study, we included PKDL patients with Macular and/or Polymorphic lesion, Cured individuals and HI. Among the enrolled patients, blood samples were collected from 20 primarily confirmed PKDL patients with Macular lesions, 20 primarily confirmed PKDL patients with Polymorphic lesions, 12 Cured individuals previously suffering from PKDL and 12 Healthy individuals; collected during the period of 2015-2016, stored at -80°C. Next the CICs were purified from PKDL patients’ plasma and LC MS/MS analysis was performed using Q-ExactivePlusOrbitrap mass spectrometer. This work for the first time revealed the differential CICs proteome profile among different forms of PKDL patients as compared to their Cured and Healthy counterparts.
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