1. Cell Biology
  2. Microbiology and Infectious Disease
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Chemotactic network responses to live bacteria show independence of phagocytosis from chemo-receptor sensing

  1. Netra Pal Meena  Is a corresponding author
  2. Alan R Kimmel  Is a corresponding author
  1. National Institutes of Health, United States
Research Article
  • Cited 9
  • Views 1,315
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Cite this article as: eLife 2017;6:e24627 doi: 10.7554/eLife.24627

Abstract

Aspects of innate immunity derive from characteristics inherent to phagocytes, including chemotaxis toward and engulfment of unicellular organisms or cell debris. Ligand chemotaxis has been biochemically investigated using mammalian and model systems, but precision of chemotaxis towards ligands being actively secreted by live bacteria is not well studied, nor has there been systematic analyses of interrelationships between chemotaxis and phagocytosis. The genetic/molecular model Dictyostelium and mammalian phagocytes share mechanistic pathways for chemotaxis and phagocytosis; Dictyostelium chemotax toward bacteria and phagocytose them as food sources. We quantified Dictyostelium chemotaxis towards live gram positive and gram negative bacteria and demonstrate high sensitivity to multiple bacterially-secreted chemoattractants. Additive/competitive assays indicate that intracellular signaling-networks for multiple ligands utilize independent upstream adaptive mechanisms, but common downstream targets, thus amplifying detection at low signal propagation, but strengthening discrimination of multiple inputs. Finally, analyses of signaling-networks for chemotaxis and phagocytosis indicate that chemoattractant receptor-signaling is not essential for bacterial phagocytosis.

Article and author information

Author details

  1. Netra Pal Meena

    Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, United States
    For correspondence
    meenan@mail.nih.gov
    Competing interests
    The authors declare that no competing interests exist.
  2. Alan R Kimmel

    Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, United States
    For correspondence
    alank@helix.nih.gov
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-0533-1939

Funding

NIH Office of the Director (N/A)

  • Netra Pal Meena

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Reviewing Editor

  1. Gadi Shaulsky

Publication history

  1. Received: December 23, 2016
  2. Accepted: May 24, 2017
  3. Accepted Manuscript published: May 25, 2017 (version 1)
  4. Version of Record published: June 19, 2017 (version 2)

Copyright

This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.

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