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14,15 It is also possible that serum 1,25-hydroxyvitamin D concentration is a stronger determinant of cathelicidin production than 25-hydroxyvitamin D, because it is the main active metabolite of vitamin D and has previously been shown to correlate with serum cathelicidin levels.23 However, measurement of 25-hydroxyvitamin D is regarded as the most accurate method of determining vitamin D status because it has a serum half-life of weeks compared with the half-life of 1,25-dihydroxyvitamin D, which is less than 4?h. Moreover, 25-hydroxyvitamin D deficiency results in a compensatory increase in parathyroid hormone secretion, which increases renal 1-alpha hydroxylase activity, maintaining 1,25-dihydroxyvitamin D levels in the normal or even elevated range.11 Lower values of serum cathelicidin showed a non-significant trend to an association with selleck chemical higher 30-day mortality. This appears to be consistent with research showing that cathelicidin supplementation is protective in murine models of sepsis.24 In addition, lower serum cathelicidin levels predict increased mortality due to infections over the following year in patients undergoing haemodialysis.23 An unexpected finding was that serum cathelicidin levels did not fall after recovery from the acute admission. This contrasts with previous studies of antimicrobial peptide levels in pneumonia, which showed trends to higher defensin levels during the acute phase of illness and a fall LMTK2 after completion of therapy, although these were small studies with sample sizes of less than 20.14,15 In our cohort, there was a strong correlation between cathelicidin levels on admission and at follow up (Spearman's rho?=?0.59, P?www.selleckchem.com/products/nlg919.html are determined by factors other than acute respiratory infection. Serum beta-defensin-2 did not predict 30-day mortality in this cohort. This may be because serum levels of beta-defensin-2 may not reflect local concentrations, as it is mainly produced by epithelial leucocytes. In contrast, cathelicidin is produced by circulating neutrophils and myeloid cells in the bone marrow as well as epithelial cells. Therefore serum cathelicidin may be a better systemic marker of innate immunity than beta-defensin-2.7 As an observational study we cannot establish causal associations between 25-hydroxyvitamin D deficiency and mortality in these patients. It is possible that these are simply serum markers of frailty and poor prognosis. Vitamin D deficiency may also reflect poor underlying nutritional status.25 However, few foods in nature are rich in vitamin D, and for most people, 90% of their vitamin D requirements are met by the conversion of cholesterol precursors in the skin to vitamin D3, by solar UV-B radiation.