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Understanding these immune evasion pathways would be an important step for the development of novel anti\u2010microbial therapeutics. Here, we report a hitherto unknown mechanism by which <jats:italic>Salmonella<\/jats:italic> exploits an anti\u2010inflammatory pathway in human immune cells to obtain survival advantage. We show that <jats:italic>Salmonella enterica<\/jats:italic> serovar Typhimurium strain 4\/74 significantly (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0\u00b705) increased expression of <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and surface protein of the type 1 receptor (<jats:styled-content style=\"fixed-case\">VPAC<\/jats:styled-content>1) for anti\u2010inflammatory vasoactive intestinal peptide (<jats:styled-content style=\"fixed-case\">VIP<\/jats:styled-content>) in human monocytes. However, we also show that <jats:italic>S<\/jats:italic>.\u00a0Typhimurium induced retrograde recycling of <jats:styled-content style=\"fixed-case\">VPAC<\/jats:styled-content>1 from early endosomes to Rab11a\u2010containing sorting endosomes, associated with the Golgi apparatus, and anterograde trafficking via Rab3a and calmodulin 1. Expression of Rab3a and calmodulin 1 were significantly increased by <jats:italic>S<\/jats:italic>.\u00a0Typhimurium infection and W\u20107 (calmodulin antagonist) decreased <jats:styled-content style=\"fixed-case\">VPAC<\/jats:styled-content>1 expression on the cell membrane while <jats:styled-content style=\"fixed-case\">CALP<\/jats:styled-content>\u20101 (calmodulin agonist) increased <jats:styled-content style=\"fixed-case\">VPAC<\/jats:styled-content>1 expression (<jats:italic>P\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0\u00b705). When infected monocytes were co\u2010cultured with <jats:styled-content style=\"fixed-case\">VIP<\/jats:styled-content>, a significantly higher number of <jats:italic>S<\/jats:italic>.\u00a0Typhimurium were recovered from these monocytes, compared with <jats:italic>S<\/jats:italic>.\u00a0Typhimurium recovered from monocytes cultured only in cell media. We conclude that <jats:italic>S<\/jats:italic>.\u00a0Typhimurium infection exploits host <jats:styled-content style=\"fixed-case\">VPAC<\/jats:styled-content>1\/<jats:styled-content style=\"fixed-case\">VIP<\/jats:styled-content> to gain survival advantage in human monocytes.<\/jats:p>","DOI":"10.1111\/imm.13107","type":"journal-article","created":{"date-parts":[[2019,8,13]],"date-time":"2019-08-13T19:14:21Z","timestamp":1565723661000},"page":"230-239","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Immune evasion by <i>Salmonella<\/i>: exploiting the <scp>VPAC<\/scp>1\/<scp>VIP<\/scp> axis in human monocytes"],"prefix":"10.1111","volume":"158","author":[{"given":"Basim","family":"Askar","sequence":"first","affiliation":[{"name":"University of Duhok Duhok Iraq"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Higgins","sequence":"additional","affiliation":[{"name":"School of Veterinary Medicine and Science University of Nottingham Nottingham UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul","family":"Barrow","sequence":"additional","affiliation":[{"name":"School of Veterinary Medicine and Science University of Nottingham Nottingham UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2970-308X","authenticated-orcid":false,"given":"Neil","family":"Foster","sequence":"additional","affiliation":[{"name":"School of Veterinary Medicine and Science University of Nottingham Nottingham UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2019,9,11]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(04)17667-8"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1586\/14737159.5.2.193"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ccm.2008.06.010"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.2008.03737.x"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.7861\/clinmedicine.9-3-256"},{"key":"e_1_2_8_7_1","first-page":"1058","article-title":"Glucocorticoid administration in sepsis and septic shock: time for a paradigm change?","volume":"80","author":"Antonucci E","year":"2014","journal-title":"Minerva Anestesiol"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-291X(85)91052-6"},{"key":"e_1_2_8_9_1","doi-asserted-by":"crossref","first-page":"1200","DOI":"10.4049\/jimmunol.162.2.1200","article-title":"Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase\u2010activation polypeptide (PACAP) protect mice from lethal endotoxemia through the inhibition of TNF\u2010\u03b1 and IL\u20106","volume":"162","author":"Delgado M","year":"1999","journal-title":"J. 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