Interleukin　17　expression　is　increased　in　children　with　Hirschsprung　disease,　which　is　characterized　by　intestinal　inflammation.　This　study　designed　to　exploit　the　characteristics　of　intestinal　inflammation　and　examine　the　correlation　of　interleukin　17　in　this　process　of　hypoganglionosis　model　established　by　benzalkonium　chloride　treatment.　Colon　sections　from　female　rats　were　treated　with　benzalkonium　chloride　to　induce　hypoganglionosis　or　with　saline　alone　as　a　sham　control.　C-reactive　protein　and　tumor　necrosis　factor-alpha　were　used　as　markers　of　inflammation.　Expression　of　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　was　assessed　in　colon　tissue　and　blood　serum　on　days　7,　14　and　21　after　treatment.　The　correlation　between　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　expression　was　estimated　using　the　Spearman＇s　rank-correlation　coefficient.　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　were　strongly　expressed　in　submucosa　and　mucosa　layers　and　serum　from　treated　animals.　The　expression　of　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　maintained　the　highest　level　at　Day　21.　Only　C-reactive　protein　and　tumor　necrosis　factor-alpha　expression　was　increased　in　control　animals　and　only　on　day　7.　Spearman＇s　rank　correlation　coefficient　was　significant　in　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　at　Day　7,　14　and　21.　Concomitant　upregulation　of　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　and　significant　positive　correlations　between　C-reactive　protein,　tumor　necrosis　factor-alpha,　and　interleukin　17　may　imply　that　interleukin　17　is　involved　in　spatio-temporal　inflammation　induced　by　benzalkonium　chloride.　(C)　2018　Elsevier　Inc.　All　rights　reserved.