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Such responses are often accompanied by significant extracellular acidosis that result in predictable transcriptional responses. In this study, we explore the mechanisms involved in inflammatory acidification as a result of PMN\u2013intestinal epithelial cell (IEC) interactions. Using recently developed tools, we revealed that PMN transepithelial migration (TEM)-associated inflammatory acidosis is dependent on the total number of PMNs present during TEM and is polarized toward the apical surface. Extending these studies, we demonstrate that physical separation of the PMNs and IECs prevented acidification, whereas inhibition of PMN TEM using neutralizing antibodies enhanced extracellular acidification. Utilizing pharmaceutical inhibitors, we demonstrate that the acidification response is independent of myeloperoxidase and dependent on reactive oxygen species generated during PMN TEM. In conclusion, inflammatory acidosis represents a polarized PMN\u2013IEC-dependent response by an as yet to be fully determined mechanism.<\/jats:p>","DOI":"10.1002\/jlb.3ma0422-742r","type":"journal-article","created":{"date-parts":[[2022,6,8]],"date-time":"2022-06-08T09:29:54Z","timestamp":1654680594000},"page":"1543-1553","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Contact-dependent, polarized acidification response during neutrophil\u2013epithelial interactions"],"prefix":"10.1093","volume":"112","author":[{"given":"Ian M","family":"Cartwright","sequence":"first","affiliation":[{"name":"Mucosal Inflammation Program, University of Colorado Anschutz Medical Campus , Aurora, Colorado, USA"},{"name":"Department of Medicine, University of Colorado Anschutz Medical Campus , Aurora, Colorado, USA"},{"name":"Rocky Mountain Regional Veterans Affairs Medical Center , Aurora, Colorado, 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