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Assaying for Inorganic Polyphosphate in Bacteria
07:20

Assaying for Inorganic Polyphosphate in Bacteria

Published on: January 21, 2019

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Polyphosphate is an extracellular signal that can facilitate bacterial survival in eukaryotic cells

Ramesh Rijal1, Louis A Cadena1, Morgan R Smith1

  • 1Department of Biology, Texas A&M University, College Station, TX 77843-3474.

Proceedings of the National Academy of Sciences of the United States of America
|December 3, 2020
PubMed

Insights

Bacterial polyphosphate enhances pathogen survival by inhibiting phagosome maturation. This molecule acts as an extracellular signal, impacting host immune cells like macrophages and Dictyostelium discoideum, thereby potentiating pathogenicity.

Area of Science:

  • Microbiology and Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Polyphosphate, a linear chain of phosphate residues, is found in diverse organisms, including pathogens.
  • Pathogenic bacteria like Mycobacterium tuberculosis accumulate polyphosphate, and its synthesis is crucial for their survival.
  • The precise role of polyphosphate in potentiating bacterial pathogenicity remains largely unknown.

Purpose of the Study:

  • To investigate the role of bacterial extracellular polyphosphate in pathogen survival and host-pathogen interactions.
  • To elucidate the mechanism by which polyphosphate influences the host immune response, specifically phagocytosis and phagosome maturation.

Main Methods:

  • Comparative analysis of polyphosphate levels and survival rates of Escherichia coli, Mycobacterium smegmatis, and Mycobacterium tuberculosis after phagocytosis by Dictyostelium discoideum and macrophages.
  • Manipulation of polyphosphate levels by altering polyphosphate kinase expression and treatment with exopolyphosphatase.
  • Assessment of phagosome acidification, lysosome activity, and early endosomal markers in host cells.
  • Investigation of the role of the polyphosphate receptor GrlD in host cell sensitivity to polyphosphate.

Main Results:

  • Bacteria accumulating extracellular polyphosphate (M. smegmatis, M. tuberculosis) exhibited better survival post-phagocytosis compared to those with low levels (E. coli).
  • Addition of extracellular polyphosphate enhanced E. coli survival, while reducing polyphosphate kinase 1 in M. smegmatis decreased survival, effects reversible by polyphosphate addition.
  • Polyphosphate inhibited phagosome acidification and lysosome activity in host cells and reduced early endosomal markers, with GrlD-deficient D. discoideum showing reduced sensitivity and increased bacterial killing.

Conclusions:

  • Bacterial polyphosphate acts as an extracellular signal that potentiates pathogenicity by inhibiting phagosome maturation in host immune cells.
  • Polyphosphate's ability to interfere with phagolysosomal processes is a key mechanism underlying enhanced pathogen survival.
  • Targeting polyphosphate metabolism or its signaling could represent a novel therapeutic strategy against bacterial infections.
Keywords:
BurkholderiaMycobacterium tuberculosisexopolyphosphatasepolyphosphatepolyphosphate kinase

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