Editor: Willem van Eden
Correlation of parasitic load with interleukin-4 response in patients with cutaneous leishmaniasis due to Leishmania tropica
Article first published online: 4 SEP 2009
© 2009 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Immunology & Medical Microbiology
Volume 57, Issue 3, pages 239–246, December 2009
How to Cite
Kumar, R., Bumb, R. A. and Salotra, P. (2009), Correlation of parasitic load with interleukin-4 response in patients with cutaneous leishmaniasis due to Leishmania tropica. FEMS Immunology & Medical Microbiology, 57: 239–246. doi: 10.1111/j.1574-695X.2009.00607.x
- Issue published online: 2 NOV 2009
- Article first published online: 4 SEP 2009
- Received 3 July 2009; revised 11 August 2009; accepted 17 August 2009.Final version published online 2 October 2009.
- parasite load;
- cutaneous leishmaniasis;
- Leishmania tropica.
We have established the association between parasite burden and localized immune response in patients with cutaneous leishmaniasis (CL) caused by Leishmania tropica. Real-time PCR was used to measure parasitic load in tissue lesions of CL patients at the pretreatment (n=26) and at the post-treatment stage (n=10). Leishmania tropica was detected in all CL lesions with a mean value of 118 357 parasites g−1 of dermal tissue. Following treatment, only one out of 10 patients showed residual parasites (100 parasites g−1 tissue). Parasite load was high (mean, 306 000 parasites g−1 tissue) in acute infections (early lesions) and low (mean, 1081 parasites g−1 tissue) in chronic infections (late lesions). Intralesional transcripts of interferon-γ, tumour necrosis factor-α, interleukin-1β (IL-1β), IL-8, IL-10 and IL-4 were investigated in early lesions (≤2 months, n=14) and late lesions (>2 months, n=15) by reverse transcriptase-PCR, where IL-4 was found to be significantly upregulated in early lesions (P<0.02). Further, the levels of parasite burden and IL-4 were distinctly correlated in various clinical forms of CL. Other cytokines were at comparable levels in early/late lesions and in different clinical forms. Upregulation of IL-4 was correlated with a higher parasite burden in early lesions of CL, which may be involved in the pathogenesis of CL by inhibiting a protective immune response.