Abstract
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.
Highlights
Leprosy continues to be the major cause of neuropathies and disabilities worldwide
Saliva samples were obtained from patients and controls, which were stratified into four groups: group 1: 116 treatment naïve leprosy patients (72 men and 44 women); group 2: 39 leprosy patients (22 men and 17 women) who had completed multidrug therapy (MDT) and were evaluated at discharge, and among them 16 were evaluated at both diagnosis and discharge; group 3: 111 household contacts (40 men and 71 women); and group 4: 11 [11] healthy endemic controls were recruited in the population with the following criteria: absence of active leprosy or leprosy in the past, no contact with leprosy patients, live in the same endemic area, older than 18 years of age, not pregnant or using immunosuppressive medication
Besides being the primary surface antigen and one of the dominant virulence factors of M. leprae, LAM shows a close relationship with leprosy reactions, since it has promoted neural damage in a mouse model by activating the complement system via membrane attack complex (MAC) [1, 6]
Summary
Leprosy continues to be the major cause of neuropathies and disabilities worldwide. Most of the infected population remains free of the disease, while a subset of infected individuals develops clinical symptoms, which are associated with the immunity of the host [1]. Difficulties persist in clinical conduct, treatment of patients, and monitoring of leprosy reactions, which may lead to nerve damage [2, 3]. Applications of Anti-LAM-Specific Salivary IgA in Leprosy. Disability in patients with recent diagnosis of leprosy and those who completed MDT treatment continues to be challenging. There is a consensus that the development and installation of neuromotor functional deficiencies and disabilities in leprosy patients are associated with morbidity and chronicity of the disease as pertains to social exclusion and stigma [4]
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