{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T10:17:33Z","timestamp":1760955453896},"reference-count":53,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2014,3,1]]},"abstract":"<jats:p>Intestinal intussusception (ISS) commonly causes intestinal obstruction in children. One mechanism that has been proposed to cause ISS is inflammation-induced alteration of intestinal motility. We investigated whether innate inflammatory factors or altered motility is required for induction of ISS by LPS. We compared rates of ISS among BALB\/c and C57BL\/6 mice, mice lacking lymphocytes or depleted of phagocytes, or mice with defects in the Toll-like receptor 4 (TLR4) signaling pathway following administration of LPS or the Ca<jats:sup>2+<\/jats:sup>analog MnCl<jats:sub>2<\/jats:sub>. At 6 or 2 h after administration of LPS or MnCl<jats:sub>2<\/jats:sub>, respectively, mice underwent image analysis to assess intestinal contraction rate or laparotomy to identify ISS. LPS-induced ISS (LPS-ISS) was observed in BALB\/c mice, but not in C57BL\/6 mice or any BALB\/c mice with disruptions of TLR4 signaling. LPS-induced serum TNF-\u03b1, IL-6, and nitric oxide (NO) and intestinal NO levels were similar in BALB\/c and C57BL\/6 mice. The rate of LPS-ISS was significantly reduced in phagocyte-depleted, but not lymphocyte-deficient, mice. Intestinal contraction rates were reduced in LPS-ISS-susceptible BALB\/c mice, but not in LPS-ISS-resistant C57BL\/6 or TLR4 mutant mice, suggesting a role for reduced intestinal contraction rate in LPS-ISS susceptibility. This was tested with MnCl<jats:sub>2,<\/jats:sub>a Ca<jats:sup>2+<\/jats:sup>antagonist that reduced intestinal contraction rates and induced ISS, irrespective of mouse strain. Therefore, LPS-ISS is initiated by innate immune signaling that requires TLR4 and phagocytes but may be independent of TNF-\u03b1, IL-6, and NO levels. Furthermore, alteration of intestinal motility, specifically, reduced intestinal contraction rate, is a key factor in the development of ISS.<\/jats:p>","DOI":"10.1152\/ajpgi.00264.2013","type":"journal-article","created":{"date-parts":[[2014,1,10]],"date-time":"2014-01-10T05:11:40Z","timestamp":1389330700000},"page":"G445-G453","source":"Crossref","is-referenced-by-count":11,"title":["Role of innate immunity and altered intestinal motility in LPS- and MnCl<sub>2<\/sub>-induced intestinal intussusception in mice"],"prefix":"10.1152","volume":"306","author":[{"given":"Kristin E.","family":"Killoran","sequence":"first","affiliation":[{"name":"Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amber D.","family":"Miller","sequence":"additional","affiliation":[{"name":"Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karen S.","family":"Uray","sequence":"additional","affiliation":[{"name":"Department of Pediatric Surgery, University of Texas Medical School at Houston, Houston, Texas;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Norman W.","family":"Weisbrodt","sequence":"additional","affiliation":[{"name":"Department of Integrative Biology and Pharmacology, University of Texas Medical School at Houston, Houston, Texas;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robia G.","family":"Pautler","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sanna M.","family":"Goyert","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Sophie Davis School of Biomedical Education, New York, New York;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nico","family":"van Rooijen","sequence":"additional","affiliation":[{"name":"Department of Molecular Cell Biology, Vrije Universiteit, Amsterdam, The Netherlands; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Margaret E.","family":"Conner","sequence":"additional","affiliation":[{"name":"Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas;"},{"name":"Michael E. 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