title: Acidic conditions in the NHE2(-/-) mouse intestine result in an altered mucosa-associated bacterial population with changes in mucus oligosaccharides.
abstract: BACKGROUND
  The mechanisms bacteria use to proliferate and alter the normal bacterial composition remain unknown. The ability to link changes in the intestinal micro-environment, such as ion composition and pH, to bacterial proliferation is clinically advantageous for diseases that involve an altered gut microbiota, such as Inflammatory Bowel Disease, obesity and diabetes. In human and mouse intestine, the apical Na(+)/H(+) exchangers NHE2 and NHE3 affect luminal Na(+), water, and pH. Loss of NHE2 results in acidic luminal pH. Since acid resistance systems in gram-positive bacteria are well documented, we hypothesize that gram-positive bacteria would increase in representation in the acidic NHE2(-/-) intestine.
  
  
  METHODS
  Intestinal ion composition was measured by fame photometry and chloridometry and pH measured electrochemically. DNA extracted from intestinal flushes or from mucosal scrapings was analyzed by qRT-PCR to examine luminal and mucosa-associated bacterial populations. Epithelial mucus oligosaccharide patterns were examined by histology with FIT-C labeled lectins .
  
  
  RESULTS
  Although total luminal and mucosa-associated bacteria were unchanged in NHE2(-/-) intestine, gram-positive bacterial phyla were increased in the mucosa-associated bacterial population in a region-specific manner. The genera Clostridium and Lactobacillus were increased in the cecum and colon which corresponded to changes in NHE2(-/-) mucus oligosaccharide composition of mannose, N-acetyglucosamine, N-acetygalactosamine and galactose.
  
  
  CONCLUSIONS
  Together these data indicate that changes in ion transport induce region-specific bacterial changes, which alter host mucus oligosaccharide patterns. These host-bacterial interactions provide a possible mechanism of niche-development and shed insight on how certain groups proliferate in changing environments and maintain their proliferation by altering the host.
authors.affiliation: Department of Molecular and Cellular Physiology, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
authors.forename: Melinda A
authors.initials: MA
authors.lastname: Engevik
authors.forename: Annelies
authors.initials: A
authors.lastname: Hickerson
authors.forename: Gary E
authors.initials: GE
authors.lastname: Shull
authors.forename: Roger T
authors.initials: RT
authors.lastname: Worrell
mesh_terms: D000143:Acids / Q000378:metabolism*; D000818:Animals; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007477:Ions / Q000737:chemistry / Q000302:isolation & purification*; D051379:Mice; D064307:Microbiota / Q000187:drug effects; D009092:Mucous Membrane / Q000187:drug effects* / Q000382:microbiology; D009093:Mucus / Q000187:drug effects / Q000378:metabolism; D009844:Oligosaccharides / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics / Q000378:metabolism*
chemical_list: D000143:Acids; D007477:Ions; D009844:Oligosaccharides; C513111:Slc9a2 protein, mouse; D017923:Sodium-Hydrogen Exchangers; D012964:Sodium