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Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus

Wei-Chuan Chang1, Mitchell R White, Patience Moyo

  • 1Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.

BMC Immunology
|December 25, 2010
PubMed
Abstract

Insights

Mannose-binding lectin (MBL) protects against influenza A virus (IAV) infection. MBL deficiency increases susceptibility, while MBL administration restores resistance, highlighting MBL's crucial role in lung immunity.

Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Mannose-binding lectin (MBL) is an innate immune molecule that inhibits influenza A virus (IAV) in vitro.
  • Human MBL deficiency is linked to increased infection susceptibility, supported by animal models showing MBL-deficient mice are susceptible to pathogens.
  • MBL's role in host defense against viral infections requires further elucidation.

Purpose of the Study:

  • To investigate the role of MBL in host defense against IAV infection in vivo.
  • To determine the mechanisms by which MBL confers protection against IAV.
  • To evaluate MBL deficiency as a risk factor and MBL as a potential therapeutic agent for IAV infection.

Main Methods:

  • Utilized wild-type (WT) and MBL-null mice to assess susceptibility to IAV infection.
  • Administered recombinant human MBL (rhMBL) to MBL-null mice to evaluate its therapeutic potential.
  • Analyzed immune cell populations (WBCs, macrophages), apoptosis markers, and soluble factors in lung tissue post-infection.
  • Investigated MBL's role in complement activation and coagulation pathways.

Main Results:

  • MBL is present in the lungs of healthy mice, and MBL-null mice exhibit increased susceptibility to IAV infection.
  • Administration of rhMBL reversed the infection phenotype in MBL-null mice, confirming MBL's protective role.
  • MBL mediates antiviral effects through complement activation and coagulation. MBL-null mice showed increased macrophage apoptosis and elevated levels of lung injury-associated soluble factors.

Conclusions:

  • MBL plays a critical role in clearing IAV and maintaining lung homeostasis.
  • MBL deficiency may represent a risk factor for IAV infection.
  • MBL holds potential as an adjunctive therapy for IAV infection.

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