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Updated: Jan 10, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Encapsulin protein MAV2054 enhances Mycobacterium avium virulence by promoting Cdc42-dependent epithelial cell

Dong Ho Kim1,2,3, I Jeong Jo1,3,4, Min Ju Kang1,3,4

  • 1Department of Microbiology, School of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.

Journal of Microbiology (Seoul, Korea)
|November 27, 2025
PubMed

Insights

A novel protein, MAV2054, from Mycobacterium avium complex (MAC) enhances bacterial invasion of lung cells. Targeting this protein could offer new treatments for chronic pulmonary MAC infections.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Mycobacterium avium complex (MAC) causes chronic lung infections.
  • Mechanisms of M. avium epithelial cell invasion are not fully understood.

Purpose of the Study:

  • To investigate the role of MAVRS09815 (MAV2054), an encapsulin protein, in M. avium pathogenesis.
  • To elucidate the molecular mechanisms of MAV2054-mediated bacterial invasion and virulence.

Main Methods:

  • Engineered recombinant M. smegmatis (Ms_2054) and M. avium MAV2054 deletion mutant (Δ2054).
  • Assessed bacterial adhesion, invasion, and intracellular survival in human epithelial cells.
  • Utilized microscopy, biochemical assays (pull-down), and a murine infection model.

Main Results:

  • MAV2054 directly binds epithelial cells and promotes invasion.
  • MAV2054-mediated invasion is cytoskeleton-dependent and involves Cdc42 activation.
  • Δ2054 mutant showed reduced bacterial load and lung inflammation in vivo.

Conclusions:

  • MAV2054 is a key virulence factor enhancing M. avium epithelial cell invasion via Cdc42-dependent cytoskeletal remodeling.
  • This encapsulin protein plays a novel role in host-pathogen interactions.
  • MAV2054 represents a potential therapeutic target for MAC pulmonary infections.
Keywords:
MAV2054Mycobacterium aviumactin cytoskeleton remodelingencapsulin nanocompartment

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