Entity

Time filter

Source Type


Singh I.,National JALMA Institute for Leprosy and Other Mycobacterial Diseases ICMR | Singh I.,Stanley Browne Laboratory | Yadav A.R.,National JALMA Institute for Leprosy and Other Mycobacterial Diseases ICMR | Mohanty K.K.,National JALMA Institute for Leprosy and Other Mycobacterial Diseases ICMR | And 6 more authors.
Microbes and Infection | Year: 2015

Autoantibodies against various components of host are known to occur in leprosy. Nerve damage is the primary cause of disability associated with leprosy. The aim of this study was to detect the level of autoantibodies and lympho-proliferative response against myelin basic protein (MBP) in leprosy patients (LPs) and their correlation with clinical phenotypes of LPs. Further, probable role of molecular mimicry in nerve damage of LPs was investigated. We observed significantly high level of anti-MBP antibodies in LPs across the spectrum and a positive significant correlation between the level of anti-MBP antibodies and the number of nerves involved in LPs. We report here that 4 B cell epitopes of myelin A1 and Mycobacterium leprae proteins, 50S ribosomal L2 and lysyl tRNA synthetase are cross-reactive. Further, M. leprae sonicated antigen hyperimmunization was responsible for induction of autoantibody response in mice which could be adoptively transferred to naive mice. For the first time our findings suggest the role of molecular mimicry in nerve damage in leprosy. © 2015 Institut Pasteur. Source


Kamble R.R.,Stanley Browne Laboratory | Shinde V.S.,Blue Peter Research Center | Madhale S.P.,Richardson Leprosy Hospital | Kamble A.A.,Richardson Leprosy Hospital | And 2 more authors.
Indian Journal of Medical Microbiology | Year: 2010

Identification of Mycobacterium leprae, which causes leprosy, is done by Ziehl Neelsen Carbol Fuchsin (ZNCF) stained slit skin smear microscopy that aids in the diagnosis and quantification of approximate bacterial load carried by the patient. We attempted M. leprae DNA extraction from 46 stained slit skin smear negative slides, using Proteinase K and SDS lysis, followed by ethanol precipitation. M. leprae specific primers (16SrRNA) were used for PCR-based amplification of DNA. We could detect M. leprae DNA in 15 (32.6%) samples. The method can be useful in the diagnosis of apparently slit skin smear negative leprosy cases. Source


Chaitanya V.S.,Mission Research | Jadhav R.S.,Government Institute of Science | Lavania M.,Mission Research | Singh M.,Lala Ramaswarup Institute of Tuberculosis and Respiratory Diseases | And 2 more authors.
International Journal of Immunogenetics | Year: 2014

The objective of this study was to investigate the association, if any, between the interleukin-17F (7488T>C) (rs763780) polymorphism and susceptibility to leprosy and to elucidate the relationship between IL-17F genotypes and clinical profile of the disease. DNA was extracted from the peripheral venous blood of leprosy cases (n = 140), which were classified as per WHO classification into paucibacillary (PB) (n = 53) and multibacillary (MB) (n = 87) categories and healthy controls (n = 84) without any signs and symptoms of leprosy. The IL-17F (7488 T/C) polymorphism was genotyped using amplification refractory mutation system - polymerase chain reaction (Allele-specific amplification). In both PB and MB categories of leprosy cases, the homozygous TT genotype frequency was significantly higher than that of the healthy controls (78.70% vs. 29.76%, P < 0.05). The heterozygous TC genotype was higher in the controls than in the leprosy cases (57.14% vs. 17.68%, P < 0.05). TT genotype was more associated with the type 1 reactional states and tuberculoid/borderline tuberculoid groups in leprosy than the TC genotype. This study reveals that the IL-17F (7488T>C) single-nucleotide polymorphism is associated with susceptibility to leprosy and polymorphism confers decrease in risk of contracting leprosy in the north Indian cohort. © 2013 John Wiley & Sons Ltd. Source


Turankar R.P.,Stanley Browne Laboratory | Lavania M.,Stanley Browne Laboratory | Chaitanya V.S.,Stanley Browne Laboratory | Sengupta U.,Stanley Browne Laboratory | And 5 more authors.
Clinical Microbiology and Infection | Year: 2014

The exact mode of transmission of leprosy is not clearly understood; however, many studies have demonstrated active transmission of leprosy around a source case. Families of five active leprosy cases and their household contacts were chosen from a high endemic area in Purulia. Fifty-two soil samples were also collected from different areas of their houses. DNA was extracted from slit-skin smears (SSS) and soil samples and the Mycobacterium leprae-specific RLEP (129 bp) region was amplified using PCR. Molecular typing of M. leprae was performed for all RLEP PCR-positive samples by single nucleotide polymorphism (SNP) typing and confirmation by DNA sequencing. SSS of these five patients and six out of the total 28 contacts were PCR positive for RLEP whereas 17 soil samples out of 52 showed the presence of M. leprae DNA. SNP typing of M. leprae from all RLEP PCR-positive subjects (patients and smear-positive contacts) and 10 soil samples showed the SNP type 1 genotype. M. leprae DNA from the five leprosy patients and the six contacts was further subtyped and the D subtype was noted in all patients and contacts, except for one contact where the C subtype was identified. Typing followed by subtyping of M. leprae clearly revealed that either the contacts were infected by the patients or both patients and contacts had the same source of infection. It also revealed that the type of M. leprae in the soil in the inhabited areas where patients resided was also of the same type as that found in patients. © 2013 The Authors Clinical Microbiology and Infection © 2013 European Society of Clinical Microbiology and Infectious Diseases. Source


Chaitanya V.S.,Stanley Browne Laboratory | Lavania M.,Stanley Browne Laboratory | Nigam A.,Stanley Browne Laboratory | Turankar R.P.,Stanley Browne Laboratory | And 4 more authors.
Immunology Letters | Year: 2013

Purpose: Cortisol levels in the circulation and at the sites of peripheral inflammation regulate type 1 (Reversal) reactions in leprosy akin to delayed type hypersensitivity reactions (DTH). In this study we determine the extent to which the differential mRNA expression of genes encoding cortisone-cortisol shuttle enzymes (11 β hydroxysteriod dehydrogenase I & II (11 β HSD I & II)), circulatory levels of proinflammatory cytokines (IL-6, IL-7, IP-10, IL-17F, IL-23, TNF-α, IL-1β, PDGF BB and CRP) and cortisol are associated with development of type 1 reactions in leprosy. Methods: Urine, blood and incisional skin biopsy samples from site of lesions were collected from 49 newly diagnosed untreated leprosy cases in T1R and 51 cases not in reaction (NR). mRNA expression levels of genes encoding 11 β HSD I & II in skin biopsy samples were determined by realtime PCR. Cortisol levels from the lesional skin biopsies, serum and urine samples and serum proinflammatory cytokine levels were measured using ELISA. Results: The mean expression ratios of 11 β HSD I & II are significantly lower in leprosy cases with T1R when compared to the NR leprosy cases. Cortisol levels in lesional skin biopsies and in urine are significantly lower (p=0.001) in leprosy cases with T1R. Serum cytokine levels of IP-10, IL-17F, IL-IL-6 and TNF-α are significantly higher (p<. 0.05) in leprosy cases with T1R when compared the NR leprosy cases. Conclusion: Our study indicated an association of urinary and lesional skin cortisol levels with the manifestation of T1R in leprosy. IP-10, IL-17F, IL-6 and TNF-α can be potential prognostic serological markers and gene expression markers for early detection of type 1 reactions in leprosy. © 2013 Elsevier B.V. Source

Discover hidden collaborations