Ekspresi Caspase-3 sebagai Petanda Apoptosis Makrofag Lesi Kulit Penderita Kusta Tipe Pausibasiler dan Multibasiler

Anggun P Yuniaswan; Santoso Basuki; Delya Widasmara

doi:10.19184/pk.v7i1.17588

Anggun P Yuniaswan Department of Dermatovenereology, Faculty of Medicine, Universitas Brawijaya/dr. Saiful Anwar Hospital
Santoso Basuki Department of Dermatovenereology, Faculty of Medicine, Universitas Brawijaya/dr. Saiful Anwar Hospital
Delya Widasmara Department of Dermatovenereology, Faculty of Medicine, Universitas Brawijaya/dr. Saiful Anwar Hospital

DOI: https://doi.org/10.19184/pk.v7i1.17588

Abstract

Macrophage and Schwann cells are target cell on leprosy disease, where apoptotic is assumed as one of elimination mechanism of macrophage previously infected by M.leprae. Several study showed various result in apoptotic on leprosy disease. Apoptotic level can be evaluated by observing caspase-3 activity, an executioner caspase on cell death. This study is aimed to observe the relationship of caspase-3 expression with paucibacillary and multibacillary types of leprosy. We used observational analytic and cross sectional study with consecutive sampling method. The subject was leprosy patient which had been diagnosed on dermatovenereology division outpatient clinic Saiful Anwar Hospital, and fullfilled the inclusion-exclusion criteria. Total subject was 19 persons (11 multibacillary and 8 paucibacillary). Sampling was taken with punch biopsy on skin lession, followed by immunohistochemical staining with caspase-3 antibody, and caspase-3 expression was measured by ImmunoRatio method. Comparation test revealed significant difference (p<0.05%) between caspase-3 expression mean on paucibacillary patient (84.46%) compared to multibacillary patient (65.39%). Pearson correlation test revealed caspase-3 expression tend to be higher in paucibacillary patient than multibacillary (coefficient correlation -0.759). In conclusion, there is a significance relationship between caspase-3 expression with leprosy type.

References

[1] World Health Organization. Global strategy for further reducing the leprosy burden and sustaining leprosy control activities 2006-2010. 2006. Operational Guidelines. Geneva: World Health Organization.
[2] Makino M. Host Defense Against M.leprae.: Leprosy, Science Working Towards Dignity. 2011. Editor: Masanao M, Masanori M, Masamichi G dan Kentaro H. Tokai. Japan University Press. Chapter 7
[3] Mustafa T, Bjune TG, Jonsson R, Pando RH, Nilsen R. Increased expression of fas ligand in human tuberculosis and leprosy lesions: a potential novel mechanism of immune evasion in mycobacterial infection. 2001. Scandinavian Journal of Immunology. Dec;54(6):630e9
[4] Garrity MM, Burgart LJ, Riehle DL, et al. Identifying and Quantifying Apoptosis: Navigating Technical Pitfalls. 2013. Modern Pathology. 16(4):389-394
[5] Apriani D N, Rismayanti, Wahiduddin. Faktor Risiko Kejadian Penyakit Kusta di Kota Makassar. 2014. repository.unhas.ac.id
[6] Bhat R.M, Prakash C. Leprosy: An Overview of Pathophysiology. 2012. Interdisciplinary Perspectives on Infectious Diseases.Vol 20
[7] World Health Organization. The Leprosy Unit: Risk of relapse in leprosy. 1995. Indian Journal of Leprosy ;67:13-26
[8] Lahiri R, Randhawa B, Krahenbuhl J. Infection of Mouse Macrophages with Viable Mycobacterium leprae Does Not Induce Apoptosis. 2010. Jornal of Investigative Dermatology. JID:201
[9] Walsh, DS. Lane JE, Abalos RM, Myint KS. TUNEL and Limited Immunophenotypic Analyses of Apoptosis in Paucibacillary and Multibacillary Leprosy Lesions. 2004. Federation of European Microbiological Societies Immunology Medical Microbiology. 41 : 265–269
[10] Souza V, Nogueira M, Belone A, dkk. Analysis of Apoptosis and Bcl-2 expression in polar forms of leprosy. 2010. Federation of European Microbiological Societies Immunology Medical Microbioogy.l 60: 270–274
[11] Quaresma JA, Lima LW, Fuzii HT, Libonati RM, Pagliari C & Duarte MI. Immunohistochemical evaluation of macrophage activity and its relationship with apoptotic cell death in the polar forms of leprosy. 2010. Microbiology Pathogenesis 49: 135–140
[12] Quaresma JA, Almeida FA, Aarao TL, dkk. Transforming growth factor β and apoptosis in leprosy skin lesions: possible relationship with the control of the tissue immune response in the Mycobacterium leprae infection. 2012. Microbes and Infection 14 : 696-701
[13] Hernandez MO, Neves I, Sales JS, Carvalho DS, Sarno EN, Sampaio EP. Induction of apoptosis in monocytes by Mycobacterium leprae in vitro: a possible role for tumor necrosis factor-alpha. 2003. Immunology;109:156e64
[14] Ajith C, Gupta S, Radotra B, dkk. Study of Apoptosis in Skin Lesions of Leprosy in Relation to Treatment and Lepra Reactions. 2005. International Journal of Leprosy. Volume 73, Number 4
[15] Fukutomi Y, Maeda Y, Makino M. Apoptosis-Inducing Activity of Clofazimine in Macrophages. 2011. Antimicrobial Agents and Chemotheraphy, p. 4000–4005
[16] Andersson M, Honarvar A, Sjöstrand J, Peterson A, Karlsson JO. Decreased caspase-3 activity in human lens epithelium from posterior subcapsular cataracts. 2003. Experimental Eye Research. Feb; 76(2):175-82
[17] Bellini M F, Cury P M, Silva A E. Expression of Ki-67 Antigen and Caspase-3 Protein in Benign Lesions and Esophageal Carcinoma. 2010. Anticancer Research July. vol. 30 no. 7 2845-2849
[18] Dukers D F, Meijer C, Berge R, Vos W, Ossenkoppele G, Oudejans J. High numbers of active caspase 3–positive Reed-Sternberg cells in pretreatment biopsy specimens of patients with Hodgkin disease predict favorable clinical outcome. 2002. Blood ;100:36-42.