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Interactions of Neisseria meningitidis with human monocytes

G McNeil1, M Virji, E R Moxon

  • 1Department of Paediatrics, University of Oxford, John Radcliffe Hospital, U.K.

Microbial Pathogenesis
|February 1, 1994
PubMed

Insights

Neisseria meningitidis capsule protects against monocyte interaction and killing. Capsule-deficient bacteria expressing Opc or Opa proteins show varied interactions and increased killing, but enhanced intracellular survival.

Area of Science:

  • Microbiology
  • Immunology
  • Bacterial Pathogenesis

Background:

  • Neisseria meningitidis (Nm) is a significant human pathogen.
  • Bacterial surface structures play crucial roles in host-pathogen interactions.
  • Understanding interactions with immune cells like monocytes is key to pathogenesis.

Purpose of the Study:

  • To investigate the roles of capsule, pili, and outer-membrane proteins (Opa, Opc) of N. meningitidis in interactions with human monocytes.
  • To determine how these factors influence bacterial adherence, internalization, and survival within monocytes.

Main Methods:

  • Utilized various meningococcal isolates from different serogroups.
  • Employed clonal variants of a serogroup A strain (C751) with defined surface protein expression.
  • Conducted adherence, internalization, and phagocytic killing assays with human monocytes.

Main Results:

  • Capsule presence significantly hindered monocyte interaction and conferred resistance to phagocytic killing.
  • Pili (Class I or II) had no significant effect on monocyte interactions in capsulate strains.
  • In capsule-deficient strains, Opc and OpaBC751 expression correlated with high monocyte association, while OpaD and OpaA showed lower association; Opc+, Opa+ bacteria were killed more readily, but capsule-deficient bacteria showed greater intracellular survival.

Conclusions:

  • The bacterial capsule is a major factor preventing early interaction with monocytes and promoting resistance to killing.
  • Outer-membrane proteins Opc and Opa modulate interactions of capsule-deficient N. meningitidis with monocytes.
  • Intracellular survival of capsule-deficient meningococci within monocytes may contribute to bacterial dissemination.

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