Abstract
BackgroundAngiogenesis and lymphangiogenesis are the processes of neovascularization that evolve from preexisting blood and lymphatic vessels. There are few studies on angiogenesis and none on lymphangiogenesis in leprosy. Thus, the role of neovascularization in the pathophysiological mechanisms of the disease was studied across the spectrum of leprosy, its reactional states and its residual lesions.Methodology/Principal FindingsSeventy-six biopsies of leprosy skin lesions and seven healthy controls were selected. Fifty-five serum samples were used for the detection of CD105 by ELISA. Histological sections were stained with antibodies against CD31 (blood and lymphatic vessels), D2-40/podoplanin (lymphatic vessels), and CD105/endoglin (neovessels). Microvessels were counted in 100 high-power fields (400x) and the number of vessels was evaluated in relation to the extension of the inflammatory infiltrate (0-3), to the bacillary index (0-6) and to the clinical forms. Angiogenesis, as marked by CD31 and CD105, was observed across the leprosy spectrum, compared with the controls. Additionally, there was a positive correlation between these markers with extension of the infiltrate (p <0.0001). For D2/40, lymphangiogenesis was observed in the tuberculoid form (p <0.0001). There was no statistical significance for values of CD105 detected in plasma by ELISA.Conclusions/SignificanceAngiogenesis is present across the spectrum of leprosy and in its reactional forms. The increase in the number of vessels, as detected by CD31 and CD105 staining, is related to the extension of the inflammatory infiltrate. Samples from reactional lesions have a higher number of CD31+ and CD105+ stained vessels, which indicates their involvement in the pathophysiological mechanisms of the reactional states. The regression of lesions is accompanied by the regression of neovascularization. Drugs inhibiting angiogenesis may be relevant in the treatment of leprosy, in addition to multidrugtherapy, and in the prevention of the development of reactions.
Highlights
Leprosy is a chronic infectious disease caused by Mycobacterium leprae
Biopsies of newly diagnosed patients were allocated to the following subgroups: seven indeterminate (I), eight tuberculoid (TT), seven borderline tuberculoid (BT), nine borderline-borderline (BB), eight borderline-lepromatous (BV), seven lepromatous (LL)
Angiogenesis is the process of the formation of new vessels from preexisting vessels, and it has important roles in physiological processes such as embryogenesis as well as in pathological processes
Summary
Leprosy is a chronic infectious disease caused by Mycobacterium leprae. The bacillus has tropism for the peripheral nervous system, making leprosy a predominantly neural disease. An immunologically unstable intermediate group separates the two polar forms and is divided into three subgroups: borderline tuberculoid (BT), borderline-borderline (BB) and borderline-lepromatous (BL) These groups are classified according to clinical characteristics, skin smear bacillary index and histopathological features [1]. Reactions are the abrupt onset of cutaneo-neural lesions, which are sometimes intensive and destructive These may occur at variable times during leprosy progression. The role of neovascularization in the pathophysiological mechanisms of the disease was studied across the spectrum of leprosy, its reactional states and its residual lesions. The increase in the number of vessels, as detected by CD31 and CD105 staining, is related to the extension of the inflammatory infiltrate. Samples from reactional lesions have a higher number of CD31+ and CD105+ stained vessels, which indicates their involvement in the pathophysiological mechanisms of the reactional states. Drugs inhibiting angiogenesis may be relevant in the treatment of leprosy, in addition to multidrugtherapy, and in the prevention of the development of reactions
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