{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T12:48:57Z","timestamp":1790167737424,"version":"4.1.0"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2000,11,1]],"date-time":"2000-11-01T00:00:00Z","timestamp":973036800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2000,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>To evaluate a possible role for altered cortisol metabolism in mediating the immunoparesis associated with progressive tuberculosis (TB), we have studied the hypothalamic-pituitary-adrenal axis, and the activities of the 11 \u03b2 -hydroxysteroid dehydrogenases (11-HSDs) that interconvert active cortisol and inactive cortisone. In active pulmonary tuberculosis (PTB), the ratio of cortisol\/cortisone metabolites in 24-h urine showed a shift towards active cortisol (ratio, 1.19 \u00b1 0.1, n = 16 versus 0. 89 \u00b1 0.05 in cured pulmonary tuberculosis (CTB), n = 13, p &amp;lt; 0. 01; and 0.78 \u00b1 0.04 healthy volunteers (HV), n = 11, p &amp;lt; 0.005). Conversion of cortisone (administered as 25 mg orally) to cortisol in peripheral plasma was higher in PTB (peak 1,157 \u00b1 55 nM, n = 14 versus 862 \u00b1 50 nM in CTB, n = 10, p &amp;lt; 0.005, and 882 \u00b1 73 nM in HV, n = 10; p &amp;lt; 0.005). Cortisol\/cortisone ratio was increased in bronchoalveolar lavage fluid in PTB (7.73 \u00b1 1.48, mean \u00b1 SE, n = 13) compared with HV (4.05 \u00b1 0.38, n = 11, p &amp;lt; 0.05) but was not different in plasma (PTB, 3.25 \u00b1 0.68; HV, 4.01 \u00b1 0.92). Responses of plasma cortisol to dexamethasone, CRH stimulation, and multidose ACTH stimulation were not different. These data suggest that in pulmonary tuberculosis, central control of glucocorticoid production is normal but that peripheral metabolism, in particular in the lung, is deviated in favor of the active metabolite cortisol. This offers a possible mechanism to explain the immunoparesis observed in progressive pulmonary tuberculosis.<\/jats:p>","DOI":"10.1164\/ajrccm.162.5.9912119","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T14:25:08Z","timestamp":1365085508000},"page":"1641-1647","source":"Crossref","is-referenced-by-count":35,"title":["Increased Cortisol"],"prefix":"10.1093","volume":"162","author":[{"given":"ROBERT W.","family":"BAKER","sequence":"first","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"BRIAN R.","family":"WALKER","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"RORY J.","family":"SHAW","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"JOHN W.","family":"HONOUR","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DAVID S.","family":"JESSOP","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"STAFFORD L.","family":"LIGHTMAN","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ALIMUDDIN","family":"ZUMLA","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"GRAHAM A. W.","family":"ROOK","sequence":"additional","affiliation":[{"name":"Centre for Infectious Diseases and Department of Bacteriology, University College and Royal Free School of Medicine, London; Department of Respiratory Medicine, NHLI, Imperial College, London; Division of Molecular Pathology, University College London; Department of Medicine, University of Bristol, Bristol, United Kingdom; and Endocrinology Unit, University of Edinburgh, Edinburgh, Scotland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,11,1]]},"reference":[{"key":"2026032708332388900_B1","doi-asserted-by":"crossref","first-page":"469","DOI":"10.1016\/S0022-2143(97)90123-2","article-title":"Regulation of the human immune response during tuberculosis.","volume":"130","author":"Ellner","year":"1997","journal-title":"J Lab Clin Med"},{"key":"2026032708332388900_B2","doi-asserted-by":"crossref","first-page":"315","DOI":"10.4049\/jimmunol.158.1.315","article-title":"T-cell-derived IL-10 antagonizes macrophage function in mycobacterial infection.","volume":"158","author":"Murray","year":"1997","journal-title":"J Immunol"},{"key":"2026032708332388900_B3","doi-asserted-by":"crossref","first-page":"145","DOI":"10.1016\/S0962-8479(97)90021-6","article-title":"Examining a paradox in the pathogenesis of human pulmonary tuberculosis: immune activation and suppression\/anergy.","volume":"78","author":"Vanham","year":"1997","journal-title":"Tuber Lung Dis"},{"key":"2026032708332388900_B4","doi-asserted-by":"crossref","first-page":"107","DOI":"10.1006\/clin.1998.4528","article-title":"Ellner JJ. 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