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Fibronectin binding protein and Ca2+ play an access key role to mediate pathogenesis in Mycobacterium tuberculosis:

Prem Raj Meena1, Monu1, Laxman S Meena1

  • 1CSIR-Institute of Genomics and Integrative Biology, Council of Scientific and Industrial Research, Mall Road, Delhi, India.

Biotechnology and Applied Biochemistry
|August 15, 2015
PubMed

Insights

Mycobacterium tuberculosis fibronectin-binding proteins (FnBP) on the cell surface are key to host cell adhesion and pathogenesis. Targeting these FnBPs and calcium ion pathways offers potential therapeutic strategies against tuberculosis.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • The role of adhesive proteins on Mycobacterium tuberculosis H37Rv cell surfaces in adhesion and host interaction is not fully understood.
  • While the M. tuberculosis genome reveals fibronectin-binding proteins (FnBP) within the PE_PGRS family, their specific functions in pathogenesis remain largely unknown.

Purpose of the Study:

  • To review the M. tuberculosis entry mechanism into host cells.
  • To investigate the association of PE_PGRS-encoded FnBP with host-pathogen interactions.
  • To explore the role of calcium ions in M. tuberculosis phagocytosis and host-pathogen dynamics.

Main Methods:

  • Literature review focusing on M. tuberculosis cell surface proteins, particularly FnBP.
  • Analysis of the M. tuberculosis genome for PE_PGRS family members encoding FnBP.
  • Discussion of the influence of calcium ions on phagocytosis and host-pathogen interactions.

Main Results:

  • Fibronectin-binding proteins (FnBP) encoded by the PE_PGRS family are implicated in M. tuberculosis host cell adhesion and pathogenesis.
  • Calcium ions play a critical role in regulating calcium trafficking during phagocytosis, influencing host-pathogen interactions.
  • FnBP may contribute to antigenic variation, potentially modulating the host immune response.

Conclusions:

  • M. tuberculosis entry into host cells involves complex mechanisms, including FnBP-mediated adhesion and calcium ion dynamics.
  • Targeting M. tuberculosis FnBP and inhibiting specific adhesion pathways presents a promising therapeutic avenue for novel drug development.
  • Understanding the interplay between FnBP, calcium ions, and host-pathogen interactions is crucial for developing effective tuberculosis treatments.
Keywords:
M. tuberculosisPE_PGRSfibronectinfibronectin binding proteinmacrophages

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