To ascertain whether IL-26 contributes to host defense against intracellular bacteria, we studied leprosy, caused by the obligate intracellular pathogen Mycobacterium leprae, as a model.
Together, these data indicate that M. leprae induces a cell fate program which includes NUPR1 as part of the host response in the progressive form of leprosy.
This study identified three new biomarkers for leprosy (ApoA1, IL-1Ra, S100A12), and confirmed five previously described biomarkers (CCL4, CRP, IL-10, IP-10, αPGL-I IgM).
(i) In demonstrating neural granuloma, sensitivity of H and E was 48.27% and that of S100 was 100%, (ii) Morphology of nerve fragments on S100 stain for cases of leprosy was fragmented and infiltrated in 37, intact and infiltrated in 19, reduced, fragmented, and infiltrated in seven, and absent in one, (iii) There was a significant difference (<i>P</i> <0.001) in the pattern of staining of S100 on intact nerve and nerves involved by granuloma in leprosy, and (iv) The probability to differentiate between leprosy and nonleprosy granuloma was statistically significant (<i>P</i> <0.001).
Our analysis highlights the anaplerotic enzyme phosphoenolpyruvate carboxylase required for this intracellular diet of <i>M. leprae</i>, identifying this enzyme as a potential antileprosy drug target.<b>IMPORTANCE</b> Leprosy remains a major problem in the world today, particularly affecting the poorest and most disadvantaged sections of society in the least developed countries of the world.
(i) In demonstrating neural granuloma, sensitivity of H and E was 48.27% and that of S100 was 100%, (ii) Morphology of nerve fragments on S100 stain for cases of leprosy was fragmented and infiltrated in 37, intact and infiltrated in 19, reduced, fragmented, and infiltrated in seven, and absent in one, (iii) There was a significant difference (<i>P</i> <0.001) in the pattern of staining of S100 on intact nerve and nerves involved by granuloma in leprosy, and (iv) The probability to differentiate between leprosy and nonleprosy granuloma was statistically significant (<i>P</i> <0.001).
These results propose that DNA gyrase is a crucial factor for Mle growth and survival and its sensitivity to temperature may be exploited in heat-based treatment of leprosy.
These results point to the effective participation of IL-37 in the immunopathogenesis of leprosy, which is expressed in both the epidermal cells and the dermis.
This founding implicated that MAP3K14 and FMNL1 were susceptibility genes for leprosy, which suggested the involvement of macrophage targeting and NF-κB pathway in the development of leprosy.
This founding implicated that MAP3K14 and FMNL1 were susceptibility genes for leprosy, which suggested the involvement of macrophage targeting and NF-κB pathway in the development of leprosy.
Thus, AKR1B10 is overexpressed on the lepromatous side (BL and LL) in samples that are in regression, especially type 2 reaction-associated lesions, rendering it a potential marker of type 2 reactional episodes of leprosy and a target of drugs against reactional episodes.
By using the population attributable fraction, we have shown that HIF1A and LACC1 are the major genes with missense variants contributing to leprosy risk in our study groups.
The results lead us to suggest a regulatory role for CR1 polymorphisms on mRNA and sCR1 levels, with haplotype-specific effects increasing susceptibility to leprosy, probably by enhancing parasite phagocytosis and inflammation.
Our results suggest that the identified MPZ and MBL2 gene mutations are associated with leprosy in a Colombian population, which correlates with MPZ and MBL2 protein function, and increase the risk of M. leprae infection in leprosy-patients' family members.
From this perspective, we outline how the co-inhibitory molecules PD-1, PD-L1, and Th1/Th17 versus Th2/Treg cells are balanced, how antigen-presenting cell maturation acts at different levels to inhibit T cells and modulate the development of leprosy, and how new interventions interfere with leprosy development.
This review focuses its attention on the influence of the Vitamin D Receptor and hepcidin expressions that can suggest the protection or severity of leprosy.