{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,25]],"date-time":"2026-07-25T00:36:12Z","timestamp":1784939772539,"version":"3.55.0"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2017,5,4]],"date-time":"2017-05-04T00:00:00Z","timestamp":1493856000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000288","name":"Royal Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000288","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Parasite Immunology"],"published-print":{"date-parts":[[2017,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Visceral leishmaniasis (<jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content>) in Sudan caused by <jats:italic>Leishmania donovani<\/jats:italic> is fatal in susceptible individuals if untreated. Treatment with sodium stibogluconate (<jats:styled-content style=\"fixed-case\">SSG<\/jats:styled-content>) leads to post\u2010kala\u2010azar dermal leishmaniasis (<jats:styled-content style=\"fixed-case\">PKDL<\/jats:styled-content>) in 58% of patients. Here, Affymetrix microarrays were used to identify genes differentially expressed in lymph nodes (N=9 paired samples) pre\u2010 and post\u2010treatment with <jats:styled-content style=\"fixed-case\">SSG<\/jats:styled-content>. Using the Bioconductor package <jats:italic>limma<\/jats:italic>, 438 genes from 28\u00a0869 post\u2010quality\u2010control probe sets were differentially expressed (<jats:italic>P<\/jats:italic><jats:sub>nominal<\/jats:sub>\u2264.02) post\u2010 vs pretreatment. Canonical pathway analysis using Ingenuity Pathway Analysis\u2122 identified \u201crole of nuclear factor of activated T\u2010cell in regulation of immune response\u201d (<jats:italic>P<\/jats:italic><jats:sub>nominal<\/jats:sub>=1.35\u00d710<jats:sup>\u22125<\/jats:sup>; <jats:styled-content style=\"fixed-case\">P<jats:sub>BH<\/jats:sub><\/jats:styled-content><jats:sub>\u2010adjusted<\/jats:sub>=4.79\u00d710<jats:sup>\u22123<\/jats:sup>), \u201cB\u2010cell development\u201d (<jats:italic>P<\/jats:italic><jats:sub>nominal<\/jats:sub>=2.04\u00d710<jats:sup>\u22124<\/jats:sup>; <jats:styled-content style=\"fixed-case\">P<jats:sub>BH<\/jats:sub><\/jats:styled-content><jats:sub>\u2010adjusted<\/jats:sub>=.024), \u201cFc\u03b3 receptor\u2010mediated phagocytosis in macrophages and monocytes\u201d (<jats:italic>P<\/jats:italic><jats:sub>nominal<\/jats:sub>=2.04\u00d710<jats:sup>\u22124<\/jats:sup>; <jats:styled-content style=\"fixed-case\">P<jats:sub>BH<\/jats:sub><\/jats:styled-content><jats:sub>\u2010adjusted<\/jats:sub>=.024) and \u201c<jats:styled-content style=\"fixed-case\">OX<\/jats:styled-content>40 signalling\u201d (<jats:italic>P<\/jats:italic><jats:sub>nominal<\/jats:sub>=2.82\u00d710<jats:sup>\u22124<\/jats:sup>; <jats:styled-content style=\"fixed-case\">P<jats:sub>BH<\/jats:sub><\/jats:styled-content><jats:sub>\u2010adjusted<\/jats:sub>=.025) as pathways differentially regulated post\u2010 vs pretreatment. Major network hub genes included <jats:italic><jats:styled-content style=\"fixed-case\">TP<\/jats:styled-content>53, <jats:styled-content style=\"fixed-case\">FN<\/jats:styled-content>1, <jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> BCL<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">JUN<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> SYK<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> RUNX<\/jats:styled-content>2, <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>1<\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">ACTA<\/jats:styled-content>2<\/jats:italic>. Top endogenous upstream regulators included <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20107 (<jats:italic>P<\/jats:italic>=2.28\u00d710<jats:sup>\u22126<\/jats:sup>), <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content> (<jats:italic>P<\/jats:italic>=4.26\u00d710<jats:sup>\u22126<\/jats:sup>), Amyloid Precursor Protein (<jats:italic>P<\/jats:italic>=4.23\u00d710<jats:sup>\u22125<\/jats:sup>) and <jats:styled-content style=\"fixed-case\">SPI<\/jats:styled-content>1\/<jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>.1 (<jats:italic>P<\/jats:italic>=1.17\u00d710<jats:sup>\u22127<\/jats:sup>). Top predicted chemical drug regulators included the flavonoid genistein (<jats:italic>P<\/jats:italic>=4.56\u00d710<jats:sup>\u22127<\/jats:sup>) and the quinoline alkaloid camptothecin (<jats:italic>P<\/jats:italic>=5.14\u00d710<jats:sup>\u22125<\/jats:sup>). These results contribute to our understanding of immunopathology associated with <jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content> and response to <jats:styled-content style=\"fixed-case\">SSG<\/jats:styled-content> treatment. Further replication could identify novel therapeutic strategies that improve on <jats:styled-content style=\"fixed-case\">SSG<\/jats:styled-content> treatment and reduce the likelihood of progression to <jats:styled-content style=\"fixed-case\">PKDL<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/pim.12431","type":"journal-article","created":{"date-parts":[[2017,4,3]],"date-time":"2017-04-03T21:14:05Z","timestamp":1491254045000},"source":"Crossref","is-referenced-by-count":18,"title":["Expression profiling of Sudanese visceral leishmaniasis patients pre\u2010 and post\u2010treatment with sodium stibogluconate"],"prefix":"10.1111","volume":"39","author":[{"given":"M. A. M.","family":"Salih","sequence":"first","affiliation":[{"name":"Institute of Endemic Disease University of Khartoum  Khartoum Sudan"},{"name":"Central Laboratory Ministry of Higher Education and Scientific Research  Khartoum Sudan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"Fakiola","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Cambridge  Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. A.","family":"Lyons","sequence":"additional","affiliation":[{"name":"Department of Medicine Cambridge Institute for Medical Research University of Cambridge  Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. M.","family":"Younis","sequence":"additional","affiliation":[{"name":"Institute of Endemic Disease University of Khartoum  Khartoum Sudan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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