Short Communication Polymorphism in cathelicidin gene (CAMP) that alters Hypoxia-inducible factor (HIF-1a::ARNT) binding is not associated with tuberculosis G. N. L opez Campos*, J. S. Velarde F elix† , ‡, L. Sandoval Ramírez§, S. C azares Salazar¶, A. L. Corona Nakamura**, G. Amaya Tapia†† & E. Prado Montes de Oca* , ‡‡ Summary Polymorphisms in the CAMP gene (cathelicidin) have not been tested in tuberculosis susceptibility. We tested polymorphisms rs9844812 (HIF-1a::ARNT binding site) and rs56122065 (CAMP) plus rs1800972 (DEFB1). SNP rs1800972 was associated with extra- pulmonary tuberculosis (EPTB) in a codominant model (genotype CG, P = 0.037, OR 4.82; 95% CI: 0.92–47.42; statistical power, 82%), but not PTB (P = 0.101) in a Mexican population. Introduction Only an estimated 10% of immunocompetent persons infected by Mycobacterium tuberculosis develop clini- cal signs of the disease. One possible explanation for this could be due to the role of variation in genes that control the host immune response to the bacilli (Cobat et al., 2013; El Baghdadi et al., 2013). Genetic suscep- tibility to tuberculosis is influenced by host polymor- phisms mainly in genes vitamin D receptor (VDR) (Alagarasu et al., 2009), ubiquitin–protein ligase (UBE3A), IL12, surfactant pulmonary-associated pro- tein A1 (SFTPA1) (Schurr, 2007), purinergic receptor P2X, ligand-gated ion channel 7 (P2X7) (Li et al., 2002), chemokine, CC motif, ligand 5 or RANTES (CCL5) (Selvaraj et al., 2011), V-AKT murine thymo- ma viral oncogene homolog 1 (AKT1)(Wang et al., 2010), solute carrier family 11, proton-coupled diva- lent metal ion transporter (SLC11A1) (Awomoyi et al., 2002), interleukin-12 receptor, beta-1 (1L12RB1) (Kusuhara et al., 2007), interferon-gamma (IFNG) (Ding et al., 2008), interleukin-10 (IL10) (Tso et al., 2005), tumour necrosis factor alpha (TNFA) (Stein et al., 2005) and Toll-like receptor 4 (TLR4) (Modlin, 2010). Antimicrobial peptides (APs) are components of innate immunity which show microbicidal activity against a variety of microorganisms (Selsted & Ouel- lette, 2005; Prado-Montes de Oca, 2010; Prado Mon- tes de Oca, 2013). APs are small (~12–80 aa), evolutively conserved molecules expressed mainly in epithelia and leucocytes. Cathelicidin LL-37 and b-def- ensins are very important in lung immunity (Tecle et al., 2010). Polymorphisms in the CAMP gene have not been studied in susceptibility to tuberculosis, in spite the in vitro activity of cathelicidin LL-37 against M. tuberculosis and its immunomodulatory properties (Liu et al., 2007; Martineau et al., 2007a). Also, in vi- tro studies of human b-defensin 1 have shown activity against M. tuberculosis (Fattorini et al., 2004).Our group reported an association between this severe form of the mycobacterial disease lepromatous leprosy and polymorphism rs1800972 (668 or 44 C/G) in the DEFB1 gene. The SNP alters one of five of puta- tive binding sites for NF-jB1 (p50/p105) in the non- coding strand of 5′ UTR of exon 1 (Prado-Montes de Oca et al., 2009; Prado-Montes de Oca, 2010), and it was recently found that this SNP is associated with pulmonary tuberculosis (PTB) in a Chinese Han popu- lation (Wu et al., 2012). * In silico Laboratory, Pharmaceutical and Medical Biotechnology Unit, Research Center in Technology and Design Assistance of Jali- sco State (CIATEJ, AC), National Council of Science and Technology, Guadalajara, Mexico, † Biology Academic Unit, Sinaloa Autonomous University (UAS), Culiacan, M exico, ‡ Genomic Medicine Center, Dr. Bernardo J. Gastelum Culiacan Primary Care Hospital, Health Minis- try (SS), Culiacan, Mexico, § Genetics Division, Western Biomedical Research Center, National Institute of Social Security (CIBO-IMSS), Guadalajara, Mexico, ¶ Biology and Chemistry Sciences Faculty, Sin- aloa Autonomous University (FCQB-UAS), Culiacan, Mexico, ** Infe- ctology Service, External Attention Medical Unit (UMAE), Western National Medical Center (CMNO), Specialty Hospital, National Insti- tute of Social Security (IMSS), Guadalajara, Mexico, †† Infectology Service, Primary Care Western Hospital, Health Ministry of Jalisco State (SSJ), Guadalajara, Mexico and ‡‡ Molecular Biology Labora- tory, Biosecurity Area, Pharmaceutical and Medical Biotechnology Unit, Research Center in Technology and Design Assistance of Jali- sco State (CIATEJ, AC), National Council of Science and Technology (CONACYT), Guadalajara, Mexico Received 24 May 2013; revised 01 July 2013; accepted 15 July 2013 Correspondence: Dr Ernesto Prado Montes de Oca, Laboratorio in silico, Unidad de BiotecnologíaM edica y Farmac eutica, Centro de Investigaci on y Asistencia en Tecnología y Dise~ no del Estado de Jalisco, A.C., Consejo Nacional de Ciencia y Tecnología. Av. Normalistas 800, Col. Colinas de la Normal, Guadalajara, Jalisco CP 44270 M exico. Tel: +52 33 3345 5200 ext. 1675; Fax: +52 33 3345 5200 ext. 1001; E-mail: eprado@ciatej.net.mx © 2013 John Wiley & Sons Ltd International Journal of Immunogenetics, 2013, 0,1–9 1 doi: 10.1111/iji.12080