Human Beta Defensin 1 (hbd1) Levels in Sputum and Lysate of Mononuclear Blood Cells of Drug-Sensitive and Drug-Resistant Pulmonary Tuberculosis Patients Attending a Tertiary Hospital in Ibadan, Nigeria.


Background: Mycobacterium tuberculosis (M. tb) that causes pulmonary tuberculosis (PTB) occupies the lungs, while human β-defensin-1 (hBD1) is expressed in all human epithelial tissues as one of the products of phagocytic leucocytes, especially at the site of microbial colonisation such as the lungs. The involvement of hBD1 in mycobacterial infection has not been extensively studied, thus there is the need to measure the levels of the hBD1 in mononuclear cell lysates and sputum of PTB patients at diagnosis.

Materials and Methods: Ninety participants aged between 15 and 64 years were recruited as follows: 30 newly diagnosed multi-drug-resistant TB (MDR-TB) patients and 30 newly diagnosed drug-sensitive TB patients (DS-TB) from MDR-TB Treatment centre and the Medicine Outpatient Clinic at University College Hospital (UCH) Ibadan, Nigeria. Thirty (30) non-TB apparently healthy individuals served as controls. The analytical method employed for the measurement of hBD1 in the sputum and lysate was the Enzyme-linked immunosorbent assay (ELISA). The data were expressed as mean and standard deviation, and the differences between the means were established using Student (t) test. P-value ≤ 0.05 indicated statistical significance.

Results: The mean levels of lysate and sputum hBD1 were not significantly different in newly diagnosed DS–TB patients (D0)compared with control(p > 0.05). Whereas, the mean levels of lysate and sputum hBD1 were significantly higher in newly diagnosed MDR–TB patients (M0) compared with newly diagnosed DS–TB patients (D0)or control (p < 0.05).

Conclusion: Due to the higher levels of hBD1 in the sputum and lysate of M0 than in D0, one might conclude that there is a relationship between chronicity of PTB and hBD1 level.

[1] Kumar, V., Abbas, A. K., Fausto, N., et al. (2007). Robins Basic Pathology (eighth edition), pp. 516–522. Saunders: Elsevier.

[2] World Health Organization. (2015). Global Tuberculosis Report (twentieth edition). Geneva. Retrieved from on 4 February 2016).

[3] World Health Organization. (2014). Global Tuberculosis Report (nineteenth edition). Geneva, Switzerland. Retrieved from global_report/en (accessed on 4 February 2016).

[4] Adams, L. and Woelke, G. (2014). Understanding Global Health: Tuberculosis and HIV/AIDS (twelfth edition), p. 10. New York, NY: McGraw-Hill.

[5] Gupta, A., Kaul, K., Tsolaki, A. G., et al. (2012). Mycobacterium tuberculosis; Immune evasion, latency and reactivation. Immunobiology, vol. 217, pp. 363–374.

[6] Bafica, A. and Aliberti, J. (ed.). (2012). Mechanisms of host protection and pathogen evasion of immune responses during tuberculosis, in Control of Innate and Adaptive Immune Responses During Infectious Disease. New York, NY: Springer Science, Business Media, LLC. DOI:

[7] Liu, P. T. and Modlin, R. L. (2008). Human macrophage host defence against Mycobacterium tuberculosis. Current Opinion in Immunology, vol. 20, pp. 371–376.

[8] Persson, Y. A., Blomgran-Julider, R., Rahman, S., et al. (2008). Mycobacterium tuberculosis - Induced apoptotic neutrophils trigger a pro-inflammatory response in macrophages through release of heat-shock protein 72, acting in synergy with the bacteria. Microbes and Infection, vol. 10, pp. 233–240.

[9] Zaiou, M. (2007). Multi-functional antimicrobial peptides; therapeutic targets in several human diseases. Journal of Molecular Medicine, vol. 85, pp. 317–329.

[10] Cole, A. M. and Waring, A. J. (2002). The role of defensins in lung biology and therapy. American Journal of Respiratory and Critical Care Medicine, vol. 1, pp. 249– 259.

[11] Yang, D., Biragyn, A., Kwak, L. W., et al. (2002). Mammalian defensins induced in immunity: More than just microbicidal. Trends in Immunology, vol. 23, pp. 291–296.

[12] Lehrer, R. I. and Ganz, T. (2002). Defensins of vertebrate animals. Current Opinion in Immunology, vol. 14, pp. 96–102.

[13] Dong-Min, S. and Eun-Kyeong, J. (2011). Immune Network, vol. 11, no. 5, pp. 245–252.

[14] Oppenheim, J. J., Biragyn, A., Kwak, L. W., et al. (2003). Roles of antimicrobial peptides such as defensins in innate and adaptive immunity. Annals of the Rheumatic Diseases, vol. 62, no. 2, pp. 17–21.

[15] Ganz, T. (2003). Defensins: Antimicrobial peptides in innate immunity. Nature Reviews Immunology, vol. 3, no. 9, pp. 710–720.

[16] Hiratsuka, T., Mukae, H., Iiboshi, H., et al. (2003). Increased concentrations of human β-defensins in plasma and bronchoalveolar lavage fluid of patients with diffuse panbronchiolitis. Thorax, vol. 58, pp. 425–430.

[17] Abiko, Y., Mitamura, J., Nishimura, M., et al. (1999). Pattern of expression of betadefensins in oral squamus cell carcinoma. Caneur Letter, vol. 143, pp. 37–43.

[18] Mizukawa, N., Sugiyima, K., Veno, T., et al. (1999). Levels of human defensin-1 an antimicrobial peptide in saliva of patients with oral inflammation. Oral Surgery, Oral Medicine, Oral Pathology, and Oral Radiology, vol. 87, pp. 539–543.

[19] Ertugrul, A. S., Dikilitas, A., Sahin, H., et al. (2012). Gingival crevicular fluid levels of human beta-defensins 1 and 3 in subjects with periodontitis and/or type 2 Y. diabetes mellitus: A cross-sectional study. Journal of Periodontal Research, vol. 48, no. 4, pp. 475–482.

[20] Kaltsa, G., Bamias, G., Siakavellas, S. I., et al. (2016). Systemic levels of human βdefensin 1 are elevated in patients with cirrhosis. Annals of Gastroenterology, vol. 29, pp. 63–70.

[21] Schwander, S. K., Sada, E., Torres, M., et al. (1996). T lymphocytic and immature macrophage alveolitis in active pulmonary tuberculosis. The Journal of Infectious Diseases, vol. 173, pp. 1267–1272.