Contributions of early adversity to pro-inflammatory phenotype in infancy: the buffer provided by attachment security

Attach Hum Dev. 2018 Feb;20(1):1-23. doi: 10.1080/14616734.2017.1362657. Epub 2017 Aug 11.


Adversity early in life is associated with systemic inflammation by adolescence and beyond. At present, few studies have investigated the associations between different forms of adversity and inflammation during infancy, making it difficult to specify the origins of disease vulnerability. This study examined the association between multiple forms of early adversity - socioeconomic status disadvantage, familial stress, maternal depression, and security of attachment - and individual differences in a composite measure of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and tumor necrosis factor-alpha) and the inflammatory protein C-reactive protein that were collected via saliva when (n = 49) children were 17 months old. In addition to gauging the direct effects of adversity, we also tested the hypothesis that infants' attachment relationship with their mother might buffer infants against the immunologic effects of early adversity. Results show that familial stress, maternal depression, and security of attachment were directly associated with infant salivary inflammation and that attachment status moderated the effect of maternal depression. The findings suggest that exposure to certain forms of adversity very early in life may engender a pro-inflammatory phenotype with possible life-long implications for health.

Keywords: C-reactive protein; Inflammation; early adversity; infancy; pro-inflammatory cytokines.

MeSH terms

  • Adult
  • C-Reactive Protein / analysis
  • Cytokines / metabolism*
  • Depression / psychology
  • Female
  • Humans
  • Infant
  • Inflammation Mediators / metabolism*
  • Male
  • Mother-Child Relations / psychology*
  • Mothers / psychology
  • Object Attachment*
  • Phenotype
  • Poverty*
  • Saliva / chemistry
  • Stress, Psychological / psychology*
  • Young Adult


  • Cytokines
  • Inflammation Mediators
  • C-Reactive Protein