Related Experiment Video

Updated: Oct 5, 2026

Histological Quantification to Determine Lung Fungal Burden in Experimental Aspergillosis
09:52

Histological Quantification to Determine Lung Fungal Burden in Experimental Aspergillosis

Published on: March 9, 2018

Mannose-binding lectin gene polymorphisms as a susceptibility factor for chronic necrotizing pulmonary aspergillosis

D J Crosdale1, K V Poulton, W E Ollier

  • 1Arthritis Research Campaign Epidemiology Unit, University of Manchester, Manchester, United Kingdom. dan.crosdale@sheffield.ac.uk

The Journal of Infectious Diseases
|July 28, 2001
PubMed

Insights

A mannose-binding lectin (MBL) deficiency may explain chronic necrotizing pulmonary aspergillosis (CNPA) in non-immunocompromised patients. Low MBL protein levels and specific mutations were more common in CNPA patients than controls.

Area of Science:

  • Immunology
  • Pulmonology
  • Genetics

Background:

  • Mannose-binding lectin (MBL) binds Aspergillus species in vitro.
  • Chronic necrotizing pulmonary aspergillosis (CNPA) often affects non-immunocompromised individuals.
  • The role of MBL deficiency in CNPA pathogenesis is unclear.

Purpose of the Study:

  • To investigate if MBL deficiency is associated with CNPA.
  • To determine MBL haplotype profiles in CNPA patients and controls.

Main Methods:

  • Blood samples from 11 CNPA patients and 82 controls were analyzed.
  • Polymerase chain reaction with sequence-specific primers and oligonucleotide probing was used.
  • MBL haplotype profiles, including codon 52 mutation, were determined.

Main Results:

  • Seven of ten white CNPA patients (70%) had MBL haplotypes encoding low protein levels.
  • This contrasts with 25.6% of white control subjects (P=.004).
  • The MBL codon 52 mutation was significantly more frequent in CNPA patients (P=.015).

Conclusions:

  • MBL deficiency is associated with chronic necrotizing pulmonary aspergillosis.
  • Low MBL levels and the codon 52 mutation may contribute to CNPA development.
  • Further research into MBL's role in fungal lung infections is warranted.

More Related Videos

Confocal Laser Scanning Microscopy-Based Quantitative Analysis of Aspergillus fumigatus Conidia Distribution in Whole-Mount Optically Cleared Mouse Lung15:01

Confocal Laser Scanning Microscopy-Based Quantitative Analysis of Aspergillus fumigatus Conidia Distribution in Whole-Mount Optically Cleared Mouse Lung

Published on: September 18, 2021

Related Concept Videos

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...