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4 results on '"Praveen Mathews, Varghese"'

1. A Recombinant Fragment of Human Surfactant Protein D induces Apoptosis in Pancreatic Cancer Cell Lines via Fas-Mediated Pathway

Author

Anuvinder Kaur, Muhammad Suleman Riaz, Valarmathy Murugaiah, Praveen Mathews Varghese, Shiv K. Singh, and Uday Kishore

Subjects
pancreatic cancer, innate immunity, surfactant protein D, apoptosis, immune surveillance, Immunologic diseases. Allergy, RC581-607
Abstract

Human surfactant protein D (SP-D) is a potent innate immune molecule, which is emerging as a key molecule in the recognition and clearance of altered and non-self targets. Previous studies have shown that a recombinant fragment of human SP-D (rfhSP-D) induced apoptosis via p53-mediated apoptosis pathway in an eosinophilic leukemic cell line, AML14.3D10. Here, we report the ability of rfhSP-D to induce apoptosis via TNF-α/Fas-mediated pathway regardless of the p53 status in human pancreatic adenocarcinoma using Panc-1 (p53mt), MiaPaCa-2 (p53mt), and Capan-2 (p53wt) cell lines. Treatment of these cell lines with rfhSP-D for 24 h caused growth arrest in G1 cell cycle phase and triggered transcriptional upregulation of pro-apoptotic factors such as TNF-α and NF-κB. Translocation of NF-κB from the cytoplasm into the nucleus of pancreatic cancer cell lines was observed via immunofluorescence microscopy following treatment with rfhSP-D as compared to the untreated cells. The rfhSP-D treatment caused upregulation of pro-apoptotic marker Fas, as analyzed via qPCR and western blot, which then triggered caspase cascade, as evident from cleavage of caspase 8 and 3 analyzed via western blot at 48 h. The cell number following the rfhSP-D treatment was reduced in the order of Panc-1 (~67%) > MiaPaCa-2 (~60%) > Capan-2 (~35%). This study appears to suggest that rfhSP-D can potentially be used to therapeutically target pancreatic cancer cells irrespective of their p53 phenotype.

Published
2018
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2. Innate Immune Pattern Recognition Receptors of Mycobacterium tuberculosis: Nature and Consequences for Pathogenesis of Tuberculosis

Author

Anthony G, Tsolaki, Praveen Mathews, Varghese, and Uday, Kishore

Subjects
Receptors, Pattern Recognition, Toll-Like Receptors, Humans, Tuberculosis, Mycobacterium tuberculosis, Immunity, Innate
Abstract

Innate immunity against Mycobacterium tuberculosis is a critical early response to prevent the establishment of the infection. Despite recent advances in understanding the host-pathogen dialogue in the early stages of tuberculosis (TB), much has yet to be learnt. The nature and consequences of this dialogue ultimately determine the path of infection: namely, either early clearance of M. tuberculosis, or establishment of M. tuberculosis infection leading to active TB disease and/or latent TB infection. On the frontline in innate immunity are pattern recognition receptors (PRRs), with soluble factors (e.g. collectins and complement) and cell surface factors (e.g. Toll-like receptors and other C-type lectin receptors (Dectin 1/2, Nod-like receptors, DC-SIGN, Mincle, mannose receptor, and MCL) that play a central role in recognising M. tuberculosis and facilitating its clearance. However, in a 'double-edged sword' scenario, these factors can also be involved in enhancement of pathogenesis as well. Furthermore, innate immunity is also a critical bridge in establishing the subsequent adaptive immune response, which is also responsible for granuloma formation that cordons off M. tuberculosis infection, establishing latency and acting as a reservoir for bacterial persistence and dissemination of future disease. This chapter discusses the current understanding of pattern recognition of M. tuberculosis by innate immunity and the role this plays in the pathogenesis and protection against TB.

Published
2021

3. Pathogenesis and Host Immune Response in Leprosy

Author

Hadida, Yasmin, Praveen Mathews, Varghese, Sanjib, Bhakta, and Uday, Kishore

Subjects
Mycobacterium leprae, Immunity, Cellular, Leprosy, T-Lymphocytes, Humans, Skin
Abstract

Leprosy is an ancient insidious disease caused by Mycobacterium leprae, where the skin and peripheral nerves undergo chronic granulomatous infections, leading to sensory and motor impairment with characteristic deformities. Susceptibility to leprosy and its disease state are determined by the manifestation of innate immune resistance mediated by cells of monocyte lineage. Due to insufficient innate resistance, granulomatous infection is established, influencing the specific cellular immunity. The clinical presentation of leprosy ranges between two stable polar forms (tuberculoid to lepromatous) and three unstable borderline forms. The tuberculoid form involves Th1 response, characterized by a well demarcated granuloma, infiltrated by CD4

Published
2021

4. A Recombinant Fragment of Human Surfactant Protein D induces Apoptosis in Pancreatic Cancer Cell Lines

Author

Anuvinder, Kaur, Muhammad Suleman, Riaz, Valarmathy, Murugaiah, Praveen Mathews, Varghese, Shiv K, Singh, and Uday, Kishore

Subjects
Caspase 8, Caspase 3, TOR Serine-Threonine Kinases, NF-kappa B, Apoptosis, Cell Cycle Checkpoints, Pulmonary Surfactant-Associated Protein D, Peptide Fragments, Recombinant Proteins, Pancreatic Neoplasms, Protein Transport, Cell Line, Tumor, Humans, fas Receptor, Tumor Suppressor Protein p53, Signal Transduction
Abstract

Human surfactant protein D (SP-D) is a potent innate immune molecule, which is emerging as a key molecule in the recognition and clearance of altered and non-self targets. Previous studies have shown that a recombinant fragment of human SP-D (rfhSP-D) induced apoptosis

Published
2017

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