Correlation of parasitic load with interleukin-4 response in patients with cutaneous leishmaniasis due to Leishmania tropica

被引:27
作者
Kumar, Rajesh [1 ]
Bumb, Ram Awatar [2 ]
Salotra, Poonam [1 ]
机构
[1] ICMR, Inst Pathol, New Delhi 110029, India
[2] SP Med Coll, Dept Skin VD & Leprosy, Bikaner, Rajasthan, India
来源
FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY | 2009年 / 57卷 / 03期
关键词
Leishmania; IL-4; parasite load; cutaneous leishmaniasis; PCR; Leishmania tropica; REAL-TIME PCR; AZAR DERMAL LEISHMANIASIS; IMMUNOLOGICAL DETERMINANTS; MOUSE-TISSUES; BALB/C MICE; KALA-AZAR; T-CELLS; ASSAY; INFECTION; DONOVANI;
D O I
10.1111/j.1574-695X.2009.00607.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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-gamma, tumour necrosis factor-alpha, interleukin-1 beta (IL-1 beta), 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.
引用
收藏
页码:239 / 246
页数:8
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