Abstract
Leprosy is a chronic inflammatory disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nervous system, leading to a high disability rate and social stigma. Previous studies have shown a contribution of genes encoding products of the lectin pathway of complement in the modulation of the susceptibility to leprosy; however, the ficolin-3/FCN3 gene impact on leprosy is currently unknown. The aim of the present study was to investigate if FCN3 polymorphisms (rs532781899: g.1637delC, rs28362807: g.3524_3532insTATTTGGCC and rs4494157: g.4473C>A) and ficolin-3 serum levels play a role in the susceptibility to leprosy. We genotyped up to 190 leprosy patients (being 114 (60%) lepromatous), and up to 245 controls with sequence-specific PCR. We also measured protein levels using ELISA in 61 leprosy and 73 controls. FCN3 polymorphisms were not associated with disease, but ficolin-3 levels were higher in patients with FCN3 *2B1 (CinsA) haplotype (p = 0.032). Median concentration of ficolin-3 was higher in leprosy per se (26034 ng/mL, p = 0.005) and lepromatous patients (28295 ng/mL, p = 0.016) than controls (18231 ng/mL). In addition, high ficolin-3 levels (>33362 ng/mL) were more common in leprosy per se (34.4%) and in lepromatous patients (35.5%) than controls (19.2%; p = 0.045 and p = 0.047, respectively). Our results lead us to suggest that polymorphisms in the FCN3 gene cooperate to increase ficolin-3 concentration and that it might contribute to leprosy susceptibility by favoring M. leprae infection.
Highlights
Leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nerves [1] and can cause progressive and permanent damage, if untreated
The molecular mechanisms of M. leprae infection and immune evasion are still poorly known, raising the need for studies that may contribute to a better understanding of leprosy etiology, as well as improvement in diagnosis and treatment
Ficolin-3 is a soluble molecule of the innate immune system that recognizes a wide range of pathogen-associated molecular patterns leading to complement activation and phagocytosis
Summary
Leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nerves [1] and can cause progressive and permanent damage, if untreated. Upon exposure to M. leprae, most individuals are intrinsically resistant to infection. Among those who are susceptible, infection may progresses to a wide spectrum of manifestations, with two polar forms: the tuberculoid leprosy and the lepromatous leprosy. Tuberculoid leprosy is characterized by strong cell-mediated immunity, type 1 cytokine profile, low bacillary load and localized lesions. Lepromatous leprosy is characterized by low cellular response, type 2 cytokine profile, high bacillary load and disseminated lesions [3]. There is enough evidence to suggest that susceptibility to leprosy and to different clinical manifestations is markedly influenced by host genetic factors [3,4,5,6]
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