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Infant Alveolar Macrophages Are Unable to Effectively Contain Mycobacterium tuberculosis

Anu Goenka1,2, Ian E Prise1, Emma Connolly1

  • 1Lydia Becker Institute of Immunology and Inflammation, Division of Infection, Immunity, and Respiratory Medicine, University of Manchester, Manchester, United Kingdom.

Frontiers in Immunology
|April 9, 2020
PubMed

Insights

Infant alveolar macrophages (AMϕs) show impaired antimycobacterial function against Mycobacterium tuberculosis (Mtb). This dysfunction in controlling Mtb replication and recruiting immune cells contributes to severe tuberculosis in infants.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Pediatrics

Background:

  • Infants are highly susceptible to disseminated tuberculosis (TB).
  • The underlying immunological reasons for infant vulnerability to TB remain unclear.
  • Alveolar macrophages (AMϕs) play a critical role in lung immunity against Mycobacterium tuberculosis (Mtb).

Purpose of the Study:

  • To investigate whether antimycobacterial function is impaired in infant AMϕs compared to adult AMϕs.
  • To identify molecular mechanisms contributing to increased TB severity in infants.

Main Methods:

  • Developed a method for obtaining AMϕs from healthy infants via rigid bronchoscopy.
  • Incubated infant and adult AMϕs with live virulent Mtb.
  • Assessed Mtb replication, phagocytic capacity, immunophenotype, and gene expression (RNA-Seq).

Main Results:

  • Infant AMϕs exhibited reduced ability to restrict Mtb replication compared to adult AMϕs.
  • Gene expression analysis revealed lower expression of mycobactericidal and IFNγ-induction pathway genes in infant AMϕs.
  • Infant AMϕs showed decreased expression of mononuclear cell chemokines, including CXCL9.

Conclusions:

  • Impaired antimycobacterial activity in infant AMϕs contributes to uncontrolled Mtb infection.
  • Reduced recruitment of mononuclear cells due to lower chemokine expression exacerbates TB in infants.
  • These findings elucidate mechanisms behind the more severe course of tuberculosis in early life.
Keywords:
chemokineinfantlunglysosomemacrophagetranscriptomicstuberculosis

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