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Survival and ultrastructural changes of Helicobacter pylori after phagocytosis by human polymorphonuclear leukocytes

L P Andersen1, J Blom, H Nielsen

  • 1Department of Microbiology, Rigshospitalet, University of Copenhagen, Denmark.

Insights

Phagocytes like polymorphonuclear leukocytes (PMNs) and monocytes can engulf Helicobacter pylori, but killing requires serum. PMNs effectively kill H. pylori with serum, while monocytes are less effective, suggesting other immune responses are crucial for clearing this infection.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Few studies have investigated the phagocytosis and killing of Helicobacter pylori by human polymorphonuclear leukocytes (PMNs) and monocytes.
  • Helicobacter pylori is a significant human pathogen, particularly in the gastric mucosa.

Purpose of the Study:

  • To investigate the role of PMNs and monocytes in the phagocytosis and killing of H. pylori.
  • To determine the influence of human serum on H. pylori killing by phagocytes.
  • To examine the ultrastructural changes in H. pylori following interaction with phagocytes and serum.

Main Methods:

  • Incubation of H. pylori with PMNs and monocytes in the presence or absence of non-immune and immune human serum.
  • Analysis of H. pylori killing using colony counts.
  • Assessment of ultrastructural changes via electron microscopy.

Main Results:

  • No significant killing of H. pylori was observed in the absence of serum.
  • Unopsonized H. pylori was phagocytosed by both PMNs and monocytes.
  • Immune serum significantly enhanced H. pylori killing, with PMNs being more effective than monocytes, especially at lower bacteria-to-phagocyte ratios.
  • Ultrastructural damage to H. pylori was observed with PMNs and serum, but less so with monocytes.
  • Monocyte-mediated killing was sometimes hindered by platelet aggregation around unaffected H. pylori.

Conclusions:

  • Serum components are crucial for effective phagocytosis and killing of H. pylori by PMNs and monocytes.
  • PMNs demonstrate a greater capacity for killing H. pylori compared to monocytes in the presence of serum.
  • The ineffectiveness of phagocytes in vivo, particularly given the high bacterial load in the gastric mucosa, suggests that other immune mechanisms are vital for H. pylori elimination.
  • The potential for intracellular survival of H. pylori warrants consideration in treatment strategies.

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