Enterococcus faecalis from healthy infants modulates inflammation through MAPK signaling pathways.
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.
Department of Microbiology, National University of Singapore, Singapore, Singapore; Division of Cellular and Molecular Research, National Cancer Centre Singapore, Singapore, Singapore.
Shugui
S
Wang
Infectious Diseases, Genome Institute of Singapore, Singapore, Singapore.
Martin Lloyd
ML
Hibberd
Division of Cellular and Molecular Research, National Cancer Centre Singapore, Singapore, Singapore; Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden.
Sven
S
Pettersson
Department of Microbiology, National University of Singapore, Singapore, Singapore.
Yuan Kun
YK
Lee
D000818:Animals; D018938:Caco-2 Cells; D017077:Culture Media, Conditioned / Q000737:chemistry; D013293:Enterococcus faecalis / Q000235:genetics / Q000378:metabolism*; D045325:HCT116 Cells; D019073:HT29 Cells; D006801:Humans; D007214:Indonesia; D007223:Infant; D007231:Infant, Newborn; D007249:Inflammation / Q000378:metabolism* / Q000382:microbiology*; D053583:Interleukin-1beta / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology; D007778:Lactobacillus / Q000235:genetics / Q000378:metabolism; D020935:MAP Kinase Signaling System; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010802:Phylogeny; D016133:Polymerase Chain Reaction; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D012486:Salmonella typhimurium / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D017077:Culture Media, Conditioned; D053583:Interleukin-1beta; D016209:Interleukin-8; D012336:RNA, Ribosomal, 16S; D014409:Tumor Necrosis Factor-alpha