Salivary anti-PGL IgM and IgA titers and serum antibody IgG titers and avidities in leprosy patients and their correlation with time of infection and antigen exposure.

The present work proposed to correlate serum antibody avidity and salivary antibody titers as parameters for time of infection and antigen exposure in a cohort study evaluating leprosy patients in different periods of treatment. Colorimetric enzyme-immunoassays for salivary antibodies, serum antibody IgG titers and avidities were performed in the samples. Anti-PGL-1 IgA and IgM salivary antibodies were significantly higher in multibacillar (MB-L) patients compared to normal controls (p<0.05), but not when compared to borderline tuberculoid (BT) or to paucibacillar (PB-L) patients (p>0.05). A good correlation was found between salivary anti-PGL-1 IgA and IgM levels in MB-L patients (r=0.41, p<0.01). Two out of 33 tested saliva samples from patients who had completed the drug regimen treatment presented positive salivary antibodies. Among non-treated patients, samples with low, medium or high serum IgG antibody avidity were found in similar frequencies. In patients under treatment, most of the serum samples showed low or medium IgG antibody avidity. The treated MB-L patients showed medium or high antibody avidity, except for two, who showed very low antibody avidity results. We suggest that salivary anti-PGL antibodies and serum IgG avidity could be useful for the indication of recent exposure or re-exposure to bacteria after chemotherapy.

Salivary anti-PGL IgM and IgA titers and serum antibody IgG titers and avidities in leprosy patients and their correlation with time of infection and antigen exposure

The present work proposed to correlate serum antibody avidity and salivary antibody titers as parameters for time of infection and antigen exposure in a co-hort study evaluating leprosy patients in different periods of treatment. Colorimetric enzyme-immunoassays for salivary antibodies, serum antibody IgG titers and avidities were performed in the samples. Anti-PGL-1 IgA and IgM salivary antibodies were significantly higher in multibacillar (MB-L) patients compared to normal controls (p<0.05), but not when compared to borderline tuberculoid (BT) or to paucibacillar (PB-L) patients (p>0.05). A good correlation was found between salivary anti-PGL-1 IgA and IgM levels in MB-L patients (r=0.41, p<0.01). Two out of 33 tested saliva samples from patients who had completed the drug regimen treatment presented positive salivary antibodies. Among non-treated patients, samples with low, medium or high serum IgG antibody avidity were found in similar frequencies. In patients under treatment, most of the serum samples showed low or medium IgG antibody avidity. The treated MB-L patients showed medium or high antibody avidity, except for two, who showed very low antibody avidity results. We suggest that salivary anti-PGL antibodies and serum IgG avidity could be useful for the indication of recent exposure or re-exposure to bacteria after chemotherapy.

Distinguishing features of anti-beta2 glycoprotein I antibodies between patients with leprosy and the antiphospholipid syndrome.

Anticardiolipin (ACA), anti-beta2 glycoprotein I (beta2GPI), and antiprothrombin antibodies of IgG and IgM classes were quantitated by enzyme-linked immunosorbent assays in 176 untreated leprosy patients across the histopathological spectrum. Positivity rates ranged from 21% (IgG ACA) to 30% (IgM anti-prothrombin) versus 4% in healthy controls (p <10(-2) to 10(-3)). Levels of IgM anti-beta2GPI and IgG ACA were significantly higher in lepromatous leprosy and multibacillary patient subgroups. IgG3 was the most common subclass reactive to both beta2GPI and prothrombin in selected high-titer leprosy sera, unlike antibodies from patients with the antiphospholipid syndrome (APS) largely restricted to IgG2. In leprosy patients, but not in the APS control group, there was no statistical correlation between ACA and anti-beta2GPI antibody levels. Likewise, a large fraction of anti-beta2GPI positive sera (36/45 and 28/44 for IgG and IgM, respectively) were unreactive in the standard ACA assay. Most assayed anti-beta2GPI antibodies from leprosy patients showed (i) ability to recognize both human and bovine beta2GPI immobilized on non-irradiated polystyrene plates, (ii) concentration-dependent inhibition of binding by cardiolipin, and (iii) relatively high avidity binding to fluid-phase beta2GPI, thereby differing from those found in APS. Finally, the location of the major epitopic region on the beta2GPI molecule targeted by autoantibodies was different in leprosy and APS, as assessed by direct binding to domain I- and V-deleted mutants and competition with the mouse monoclonal antibody 8C3, directed at domain I. Thus, leprosy-related antiphospholipid antibodies comprise persistent IgG and IgM anti-beta2GPI that differ from APS-related ones with respect to IgG subclass, avidity and epitope specificity, possibly reflecting distinct pathophysiological significance.