Pathology and pathogenesis of human leptospirosis: a commented review.

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Immunohistochemical detection of Lp25 and LipL32 proteins in skeletal and cardiac muscles of fatal human leptospirosis

Leptospirosis is an acute infection caused by pathogenic species of the genus Leptospira, which affects humans and animals in all world. In severe forms of the disease, kidneys, liver and lungs are the main affected organs, resulting in acute kidney injury, jaundice and pulmonary hemorrhage. Previous post-mortem studies have shown that lesions are not limited to these organs. Cardiac and striated muscle injuries have already been reported, but the pathophysiology of cardiac and skeletal lesions in leptospirosis is not fully understood. It has been suggested that the tissue damage observed in leptospirosis could be directly mediated by leptospires or by their toxic cellular components. LipL32 and Lp25 are leptospira membrane proteins with unknown functions, that are present only in pathogenic strains of Leptospira spp. Both proteins induce skeletal muscle lesions similar to those observed when normal guinea pigs are inoculated with leptospires. Through immunohistochemistry, this study showed the presence of LipL32 and Lp25 proteins on muscle cell membranes and in the underlying cytoplasm of skeletal muscles, as well as focal lesions in cardiac tissues of fatal cases of leptospirosis. Altogether, these results reinforce that both proteins can be important factors in the pathogenesis of leptospirosis

Renal Involvement in Leptospirosis: The Effect of Glycolipoprotein on Renal Water Absorption

on vasopressin (Vp) action in the guinea pig inner medullary collecting duct (IMCD). Copenhageni, GLPc, n = 5); Group II, IMCD from normal guinea-pigs in the presence of GLPc (GLPc group, n = 54); Group III, IMCD from injected animals with GLPc ip (n = 8). (GLPp, non pathogenic, 250 µg) did not alter Vp action. In Group III, GLPc (250 µg) injected intraperitoneally produced a decrease of about 20% in IMCD Aquaporin 2 expression.The IMCD Pf decrease caused by GLP is evidence, at least in part, towards explaining the urinary concentrating incapacity observed in infected guinea-pigs

IMCD water permeability.

<p>Effects of GLPc (250 µg/ml) on: 2A - Vasopressin action (Vp, 200 pg/ml, n = 5), 2B - cAMP activity (10⁻⁵ M), 2C - Forskolin action (Fors 10⁻⁹ M, n = 5), 2D - Cholera Toxin action (ChT 10⁻⁹ M, n = 6), 2E - effect of GLPp on Vp action (GLPp- 250 µg/ml, n = 5). Values are expressed as mean ± SEM. Lines connect the averages of the data for each different period of the experiments. Significant differences: * p<0.02, **p<0.01. £ p<0.05, # p<0.001.</p

Data from normal and leptospirotic guinea pigs.

<p>Values are expressed as mean±SEM. Pf- Osmotic Water Permeability, µm/s; UOsm- Urinary Osmolality, mOsm/Kg H₂O; UV- Urinary Volume ml; BUN-Blood Urea Nitrogen mg%; ngp- normal and lgp leptospirotic guinea pigs.</p>**<p>-p<0.05;</p>*<p>p<0.01 vs ngp values.</p

Western blot analysis of water transporter protein in IMCD from normal (n = 3) and injected i.p. with GLPc (n = 5) guinea pigs.

<p>3A- Western blot analysis of AQP2 protein expression showing the 29 KDa and 35–50 KDa bands and the actin band; 3B- Quantitative densitometric analysis of AQP2 protein abundance. * p<0.05 vs. control.</p

Leptospirotic guinea pig data.

<p>A- Urinary Volume (ml) and Urinary Osmolality (mOsm/Kg H₂O). Dotted bar-UOsm; Open bar-UV. B- Water permeability. Pf µm/s. Values are expressed as mean ± SEM. Significant differences: * p<0.01; ** p<0.05.</p