RT Journal Article SR Electronic T1 Paradoxical interaction between cancer and long-term postsepsis disorder: impairment of de novo carcinogenesis versus favoring the growth of established tumors JF Journal for ImmunoTherapy of Cancer JO J Immunother Cancer FD BMJ Publishing Group Ltd SP e000129 DO 10.1136/jitc-2019-000129 VO 8 IS 1 A1 Caio Abner Leite A1 Jose Mauricio Mota A1 Kalil Alves de Lima A1 Carlos Wagner Wanderley A1 Leticia Almeida Nascimento A1 Marcela Davoli Ferreira A1 Camila Meirelles Souza Silva A1 David Fernando Colon A1 Juliana Yumi Sakita A1 Vinicius Kannen A1 Paula Ramos Viacava A1 Maria Dirlei Begnami A1 Roberto Cesar Pereira Lima-Junior A1 Vladmir Claudio Cordeiro de Lima A1 Jose Carlos Alves-Filho A1 Fernando Queiroz Cunha A1 Ronaldo Albuquerque Ribeiro YR 2020 UL http://jitc.bmj.com/content/8/1/e000129.abstract AB Background Previous data have reported that the growth of established tumors may be facilitated by postsepsis disorder through changes in the microenvironment and immune dysfunction. However, the influence of postsepsis disorder in initial carcinogenesis remains elusive.Methods In the present work, the effect of postsepsis on inflammation-induced early carcinogenesis was evaluated in an experimental model of colitis-associated colorectal cancer (CAC). We also analyzed the frequency and role of intestinal T regulatory cells (Treg) in CAC carcinogenesis.Results The colitis grade and the tumor development rate were evaluated postmortem or in vivo through serial colonoscopies. Sepsis-surviving mice (SSM) presented with a lower colonic DNA damage, polyp incidence, reduced tumor load, and milder colitis than their sham-operated counterparts. Ablating Treg led to restoration of the ability to develop colitis and tumor polyps in the SSM, in a similar fashion to that in the sham-operated mice. On the other hand, the growth of subcutaneously inoculated MC38luc colorectal cancer cells or previously established chemical CAC tumors was increased in SSM.Conclusion Our results provide evidence that postsepsis disorder has a dual effect in cancer development, inhibiting inflammation-induced early carcinogenesis in a Treg-dependent manner, while increasing the growth of previously established tumors.