Anti-Lipoarabinomannan-Specific Salivary IgA as Prognostic Marker for Leprosy Reactions in Patients and Cellular Immunity in Contacts.

Leprosy causes the most common peripheral neuropathy of infectious etiology, posing an important public health problem worldwide. Understanding the molecular and immunological mechanisms of nerve damage induced by M. leprae is mandatory to develop tools for early diagnosis and preventive measures. The phenolic glycolipid 1 (PGL-1) and lipoarabinomannan (LAM) antigens are major components of the bacterial surface and are implicated on leprosy immunopathogenesis and neural damage. Although the anti-PGL-1 serum IgM is highly used for operational classification of patients, the anti-LAM salivary IgA (sIgA) has not been investigated as diagnostic or prognostic marker in leprosy. Our aim was to assess the presence of anti-LAM sIgA in leprosy patients and their contacts in order to demonstrate whether such expression was associated with leprosy reactions. Distinct patterns of anti-LAM slgA were observed among groups, which were stratified into treatment-naïve patients (116), patients who completed multidrug therapy-MDT (39), household contacts (111), and endemic controls (11). Both anti-LAM sIgA and anti-PGL-I serum IgM presented similar prognostic odds toward leprosy reactions [(odds ratio) OR = 2.33 and 2.78, respectively]. Furthermore, the anti-LAM sIgA was highly correlated with multibacillary (MB) forms (OR = 4.15). Contrarily, among contacts the positive anti-LAM sIgA was highly correlated with those with positive Mitsuda test, suggesting that the presence of anti-LAM slgA may act as an indicator of cellular immunity conferred to contacts. Our data suggest that anti-LAM slgA may be used as a tool to monitor patients undergoing treatment to predict reactional episodes and may also be used in contacts to evaluate their cellular immunity without the need of Mitsuda tests.

DNAhsp65 Vaccine as Therapy against Paracoccidioidomycosis.

The conventional treatment for fungal diseases usually shows long periods of therapy and the high frequency of relapses and sequels. New strategies of the treatment are necessary. We have shown that the Mycobacterium leprae HSP65 gene can be successfully used as therapy against murine Paracoccidioidomycosis (PCM). Here, we described the methodology of DNAhsp65 immunotherapy in mice infected with the dimorphic fungus Paracoccidioides brasiliensis, one of PCM agent, evaluating cytokines levels, fungal burden, and lung injury. Our results provide a new prospective on the immunotherapy of mycosis.

B-cell immune responses in HIV positive and HIV negative patients with tuberculosis evaluated with an ELISA using a glycolipid antigen.

The diagnostic value of the PGL-Tb1 enzyme-linked immunosorbent assays (ELISA) was established following a survey study using sera from 220 Tuberculosis patients (including 69 HIV coinfected) and 324 controls. A higher percentage (76.8%) of the HIV-seropositive compared to the HIV-seronegative (58.9%) TB patients were ELISA positive (p=0.02) with a specificity of 94%. In HIV-positive TB patients, ELISA sensitivity was identical for all sites of disease and antibody levels were not affected by the CD4+ counts, PPD results, age or bacterial yield. Combining data for both the smear microscopy and ELISA maximized sensitivity. The kinetics of anti-PGL-Tb1 antibody was evaluated in cohort studies using sera collected before, during and after treatment for clinical TB for 79 TB patients (including 39 HIV coinfected). Statistically significant ELISA signals were observed in 51.3% of HIV-seropositive TB patients prior to the diagnosis of clinical TB and elevated antibody levels persisting 18 months after the end of antituberculous chemotherapy. Asymptomatic development of antibody also occurred in 22.7% of a cohort of 44 HIV-positive patients with a high risk of tuberculosis, but no correlation was found between persisting elevated antibody levels and progression to active disease. This antibody response in absence of disease, might reflect the control of an incipient tuberculosis infection by antituberculous prophylaxis or through an improved protective immune response associated with antiretroviral therapy.