title: Histamine-2 receptor blockers alter the fecal microbiota in premature infants.
abstract: OBJECTIVE
  Bacterial colonization is considered a major risk factor for necrotizing enterocolitis (NEC). The objective of the present study was to test the hypothesis that histamine-2 receptor (H2-) blockers alter colonic bacterial colonization by analyzing and comparing the fecal microbiota in premature infants with and without H2-blocker therapy using sensitive molecular biological techniques.
  
  
  METHODS
  Seventy-six premature infants ≤1500 g or <34 weeks gestation were enrolled in this case-controlled, cross-sectional study. Stool samples were collected from 25 infants receiving H2-blockers and 51 babies who had never received them. Following DNA extraction and PCR amplification of 16S rRNA, 454 pyrosequencing was undertaken and the resulting sequences were subjected to comparison with published sequence libraries.
  
  
  RESULTS
  Proteobacteria and Firmicutes were the major phyla contributing to fecal microbial communities. Microbial diversity was lower, relative abundance of Proteobacteria (primarily of the family Enterobacteriaceae) was increased, whereas that of Firmicutes was decreased in the stools of infants receiving H2-blockers compared with those who had never received them.
  
  
  CONCLUSIONS
  Although not designed to look specifically at the effect of H2-blockers on the incidence of NEC, our study suggests that their use lowers fecal microbial diversity and shifts the microfloral pattern toward Proteobacteria. These alterations in fecal microbiota may predispose the vulnerable immature gut to necrotizing enterocolitis and suggest prudence in the use of H2-blockers in the premature infant.
authors.affiliation: Department of Pediatrics, Division of Neonatology, Louisiana State University Health Sciences Center, New Orleans, LA 70118, USA. rwetze@lsuhsc.edu
authors.forename: Raegan W
authors.initials: RW
authors.lastname: Gupta
authors.forename: Lynn
authors.initials: L
authors.lastname: Tran
authors.forename: Johana
authors.initials: J
authors.lastname: Norori
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Ferris
authors.forename: A Murat
authors.initials: AM
authors.lastname: Eren
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Taylor
authors.forename: Scot E
authors.initials: SE
authors.lastname: Dowd
authors.forename: Duna
authors.initials: D
authors.lastname: Penn
mesh_terms: D016022:Case-Control Studies; D002657:Child Development; D003430:Cross-Sectional Studies; D020345:Enterocolitis, Necrotizing / Q000453:epidemiology / Q000382:microbiology / Q000517:prevention & control; D005243:Feces / Q000382:microbiology*; D005260:Female; D006090:Gram-Negative Bacteria / Q000187:drug effects* / Q000254:growth & development / Q000302:isolation & purification; D006094:Gram-Positive Bacteria / Q000187:drug effects* / Q000254:growth & development / Q000302:isolation & purification; D006635:Histamine H2 Antagonists / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007235:Infant, Premature, Diseases / Q000453:epidemiology / Q000382:microbiology / Q000517:prevention & control; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000254:growth & development / Q000382:microbiology; D007422:Intestines / Q000187:drug effects* / Q000254:growth & development / Q000382:microbiology; D008137:Longitudinal Studies; D008145:Louisiana / Q000453:epidemiology; D008297:Male; D020560:Proteobacteria / Q000187:drug effects / Q000254:growth & development / Q000302:isolation & purification; D012307:Risk Factors
chemical_list: D006635:Histamine H2 Antagonists