{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T11:41:42Z","timestamp":1777462902449,"version":"3.51.4"},"reference-count":41,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,10,15]],"date-time":"2013-10-15T00:00:00Z","timestamp":1381795200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/3.0\/"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2013,11]]},"abstract":"Background and Purpose<\/jats:title>Immune challenge of mice with B<\/jats:styled-content>acille C<\/jats:styled-content>almette\u2013G<\/jats:styled-content>u\u00e9rin (BCG<\/jats:styled-content>) has been reported to cause transient weight loss and a behavioural sickness response. Although BCG<\/jats:styled-content>\u2010induced depression involves the kynurenine pathway, weight loss occurs independently of this factor. Because neuropeptide Y<\/jats:styled-content> (NPY<\/jats:styled-content>) and peptide YY<\/jats:styled-content> (PYY<\/jats:styled-content>) are involved in the regulation of food intake, we hypothesized that they play a role in the BCG<\/jats:styled-content>\u2010induced weight loss.<\/jats:p><\/jats:sec>Experimental Approach<\/jats:title>Male wild\u2010type, PYY<\/jats:styled-content> knockout (PYY<\/jats:styled-content>\u2212\/\u2212), NPY<\/jats:styled-content> knockout (NPY<\/jats:styled-content>\u2212\/\u2212) and NPY<\/jats:styled-content>\u2212\/\u2212;PYY<\/jats:styled-content>\u2212\/\u2212 double knockout mice were injected with vehicle or BCG<\/jats:styled-content> (approximately 108<\/jats:sup> colony\u2010forming units per mouse), and their weight, locomotion, exploration and ingestion were recorded for 2 weeks post\u2010treatment.<\/jats:p><\/jats:sec>Key Results<\/jats:title>Deletion of PYY<\/jats:styled-content> and NPY<\/jats:styled-content> aggravated the BCG<\/jats:styled-content>\u2010induced loss of body weight, which was most pronounced in NPY<\/jats:styled-content>\u2212\/\u2212;PYY<\/jats:styled-content>\u2212\/\u2212 mice (maximum loss: 15%). The weight loss in NPY<\/jats:styled-content>\u2212\/\u2212;PYY<\/jats:styled-content>\u2212\/\u2212 mice did not normalize during the 2 week observation period. BCG<\/jats:styled-content> suppressed the circadian pattern of locomotion, exploration and food intake. However, these changes took a different time course than the prolonged weight loss caused by BCG<\/jats:styled-content> in NPY<\/jats:styled-content>\u2212\/\u2212;PYY<\/jats:styled-content>\u2212\/\u2212 mice. The effect of BCG<\/jats:styled-content> to increase circulating IL\u20106 (measured 16 days post\u2010treatment) remained unaltered by knockout of PYY<\/jats:styled-content>, NPY<\/jats:styled-content> or NPY<\/jats:styled-content> plus PYY<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusions and Implications<\/jats:title>These data show that NPY<\/jats:styled-content> and PYY<\/jats:styled-content> are both required to protect from the action of BCG<\/jats:styled-content>\u2010evoked immune challenge to cause prolonged weight loss and disturb energy balance. The findings attest to an important role of NPY<\/jats:styled-content> and PYY<\/jats:styled-content> in orchestrating homeostatic reactions to infection and immune stimulation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.12354","type":"journal-article","created":{"date-parts":[[2013,8,29]],"date-time":"2013-08-29T02:12:49Z","timestamp":1377742369000},"page":"1014-1026","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Neuropeptide Y<\/scp> and peptide YY<\/scp> protect from weight loss caused by B<\/scp>acille C<\/scp>almette\u2013G<\/scp>u\u00e9rin in mice"],"prefix":"10.1111","volume":"170","author":[{"given":"Evelin","family":"Painsipp","sequence":"first","affiliation":[{"name":"Research Unit of Translational Neurogastroenterology Institute of Experimental and Clinical Pharmacology Medical University of Graz Graz Austria"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin 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