03453nas a2200529 4500000000100000008004100001260000900042653001500051653001000066653000900076653002200085653001700107653001100124653002500135653001000160653001300170653001100183653001100194653001700205653001200222653002200234653000900256653002700265653002100292653001600313653003500329653005000364653002800414653002600442653000900468653001600477100001400493700001100507700001700518700001500535700001600550700001000566700001400576700001500590245009200605856007700697300001100774490000600785050001500791520210300806022001402909 2013 d c201310aAdolescent10aAdult10aAged10aAged, 80 and over10aAntigens, CD10aBiopsy10aCase-Control Studies10aChild10aEndoglin10aFemale10aHumans10aInflammation10aleprosy10aLymphangiogenesis10aMale10aMembrane Glycoproteins10aMicrocirculation10aMiddle Aged10aNeovascularization, Pathologic10aPlatelet Endothelial Cell Adhesion Molecule-110aReceptors, Cell Surface10aRetrospective Studies10aSkin10aYoung Adult1 aSoares CT1 aRosa P1 aTrombone APF1 aFachin LRV1 aGhidella CC1 aUra S1 aBarreto J1 aBelone AFF00aAngiogenesis and lymphangiogenesis in the spectrum of leprosy and its reactional forms. uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765444/pdf/pone.0074651.pdf ae746510 v8 aSOARES20133 a
BACKGROUND: Angiogenesis 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 FINDINGS: Seventy-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/SIGNIFICANCE: Angiogenesis 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.
a1932-6203