Enterococcus faecalis from healthy infants modulates inflammation through MAPK signaling pathways

PLoS One. 2014 May 15;9(5):e97523. doi: 10.1371/journal.pone.0097523. eCollection 2014.

Abstract

Colonizing commensal bacteria after birth are required for the proper development of the gastrointestinal tract. It is believed that bacterial colonization pattern in neonatal gut affects gut barrier function and immune system maturation. Studies on the development of faecal microbiota in infants showed that the neonatal gut was first colonized with enterococci followed by other microbiota such as Bifidobacterium. Other studies showed that babies who developed allergy were less often colonized with Enterococcus during the first month of life as compared to healthy infants. Many studies have been conducted to elucidate how bifidobacteria or lactobacilli, some of which are considered probiotic, regulate infant gut immunity. However, fewer studies have been focused on enterococi. In our study, we demonstrate that E. faecalis, isolated from healthy newborns, suppress inflammatory responses activated in vivo and in vitro. We found E. faecalis attenuates proinflammatory cytokine secretions, especially IL-8, through JNK and p38 signaling pathways. This finding shed light on how the first colonizer, E.faecalis, regulates inflammatory responses in the host.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caco-2 Cells
  • Culture Media, Conditioned / chemistry
  • Enterococcus faecalis / genetics
  • Enterococcus faecalis / metabolism*
  • HCT116 Cells
  • HT29 Cells
  • Humans
  • Indonesia
  • Infant
  • Infant, Newborn
  • Inflammation / metabolism*
  • Inflammation / microbiology*
  • Interleukin-1beta / metabolism
  • Interleukin-8 / metabolism
  • Intestinal Mucosa / metabolism
  • Intestines / microbiology
  • Lactobacillus / genetics
  • Lactobacillus / metabolism
  • MAP Kinase Signaling System*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Phylogeny
  • Polymerase Chain Reaction
  • RNA, Ribosomal, 16S / genetics
  • Salmonella typhimurium / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Culture Media, Conditioned
  • Interleukin-1beta
  • Interleukin-8
  • RNA, Ribosomal, 16S
  • Tumor Necrosis Factor-alpha