Suppression of autologous peripheral blood mononuclear cell proliferation by alveolar macrophages from young infants

Clin Exp Immunol. 2002 May;128(2):313-7. doi: 10.1046/j.1365-2249.2002.01848.x.

Abstract

Maintenance of lung homeostasis involves a complex interaction between T lymphocytes and alveolar macrophages (AM), in which AM suppress pulmonary T cell proliferation to antigenic stimuli. To assess whether AM-mediated suppression is attenuated in healthy young infants, AM and peripheral blood mononuclear cells (PBMC) were sampled prior to elective surgery. Children were divided into <4 months of age (Group I) and >4 months (Group II). Autologous PBMC and AM were co-cultured in vitro with phytohaemaglutinin (PHA) at AM : PBMC ratios ranging from 2:1 to 1 : 5. Methyl-tritiated thymidine was added after 48 h and uptake determined at 72 h. Percentage suppression or enhancement of PBMC proliferation by AM was determined relative to proliferation of PBMC with PHA. To determine the role of soluble factors of suppression, cell-free supernatants from paediatric AM and PBMC co-cultures were added to PHA-stimulated adult PBMC. The median age was 3 months for Group I (n = 9) and 7 years 2 months (n = 13) for Group II. Percentage suppression of PBMC proliferation was attenuated in Group I (versus Group II) at AM : PBMC ratios of 2:1 (median 78 versus 92, P< 0 x 05) and 1 : 1 (45 versus 87, P< 0 x 01). Cell-free supernatants from Groups I and II suppressed proliferation of adult PBMC, but there was no difference in suppression between the age groups. We conclude that suppression of autologous PHA-stimulated PBMC proliferation by AM is attenuated in young infants, and this immaturity is not explained by reduced release of soluble factors.

MeSH terms

  • Adolescent
  • Adult
  • Cell Communication / immunology*
  • Cell Division / drug effects
  • Cell Division / immunology
  • Child, Preschool
  • Coculture Techniques
  • Humans
  • Infant
  • Leukocytes, Mononuclear / immunology*
  • Leukocytes, Mononuclear / pathology
  • Macrophages, Alveolar / immunology*
  • Macrophages, Alveolar / pathology
  • Phytohemagglutinins / pharmacology

Substances

  • Phytohemagglutinins