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Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
Published on: October 25, 2017
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Calcium Signaling Commands Phagosome Maturation Process
Gourango Pradhan1,2, Philip Raj Abraham1, Rohini Shrivastava1,2
1a Laboratory of Molecular Cell Biology , Centre for DNA Fingerprinting and Diagnostics (CDFD) , Hyderabad , India.
International Reviews of Immunology
|May 24, 2019
Summary
Calcium signaling regulates phagosome-lysosome fusion, a key immune response. Intracellular pathogens exploit calcium pathways to block this fusion, offering potential therapeutic targets for infectious diseases.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Phagosome-lysosome (P-L) fusion is a critical host immune response.
- Calcium (Ca2+) signaling is increasingly recognized for its role in phagosome maturation.
- Ca2+ influences actin rearrangement, NADPH oxidase activation, and protein kinase C (PKC) activity.
Purpose of the Study:
- To review the mechanisms by which Ca2+ signals influence P-L fusion.
- To discuss pathogen strategies for manipulating Ca2+ pathways to inhibit P-L fusion.
- To highlight the therapeutic potential of targeting Ca2+ signaling in infectious diseases.
Main Methods:
- Literature review focusing on Ca2+ signaling in phagosome maturation.
- Analysis of Ca2+-dependent pathways including ROS, actin, and PKC.
- Examination of pathogen-specific subversion mechanisms.
Main Results:
- Ca2+ signaling orchestrates key cellular processes essential for P-L fusion.
- Intracellular pathogens actively modulate Ca2+ pathways to evade immune clearance.
- Specific pathogen strategies involve disrupting Ca2+-dependent regulation of ROS, actin, and PKC.
Conclusions:
- Understanding Ca2+ signaling's role in P-L fusion is crucial for host defense.
- Pathogen manipulation of Ca2+ pathways represents a significant challenge to immunity.
- Targeting Ca2+ signaling pathways offers a promising avenue for novel anti-infective therapies.
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