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Maintenance of enterocyte activity during extracellular acidosis requires functional sodium/proton exchangers (NHE), which are present at both basolateral and apical surfaces. Necrotizing enterocolitis is characterized by systemic hypoperfusion, metabolic acidosis, and the apical to basolateral translocation of endotoxin (lipopolysaccharide [LPS]). We hypothesized that LPS differentially impairs NHE activity at the basolateral or apical domains of enterocytes, leading to cellular acidification, and explored the mechanisms involved.

Experimental necrotizing enterocolitis (NEC) was induced in newborn rats using a combination of gavage feeds and hypoxia. NHE isoforms were assessed in primary and cultured enterocytes by Western blot analysis and by confocal microscopy in the presence or absence of LPS. NHE activity was detected by single-cell fluorescent ratiometric imaging with the …