Abstract
PROBLEM STATEMENT: Tissue Inhibitor of Metalloproteinases-1 (TIMP-1) and its cognate targets, the Matrix Metalloproteinases (MMPs), were differentially expressed in human brain samples with or without HIV-1 infection or HIV-1 Encephalitis (HIVE). APPROACH: A through literature review demonstrated that cell culture models of Central Nervous System (CNS) cell types had been used to illustrate the intricate temporal patterns of TIMP-1/MMP expression, regulated by a variety of inflammatory cytokines. RESULTS: As MMPs and TIMP-1 can significantly altered the extracellular environment and cell signaling, the differential regulation of TIMP-1/MMP expression in neuroinflammation can impact neuronal function and survival in disease conditions. TIMP-1 pro-survival effects had been demonstrated in a variety of cell types including CNS neurons, protecting cells from a wide range of stress and insults. TIMP-1, also known to interact with non-MMP targets, altered cell behavior. In this review, we discussed the possibility that the upregulation of TIMP-1 by glia in acute neuroinflammation may be a neuroprotective response. CONCLUSION: It will be important to delineate the effects of TIMP-1 on neurons and identify receptors and downstream signaling pathways, in order to evaluate TIMP-1 as a therapeutic strategy for neuroinflammatory and neurodegenerative diseases.
Highlights
Leprosy is a chronic infectious disease caused by Mycobacterium leprae, an acid-fast bacillus that presents a peculiar tropism for peripheral nerves and the skin
Serum antibody titers: Serum anti-PGL-1 IgM antibody was significantly higher in leprosy patients compared to healthy controls (p
When the analysis was made based on the operational classification in the MB patients (n = 21) were found to have higher salivary (IgA) and serum anti-PGL-1 values than in PB patients (n = 09)
Summary
Leprosy is a chronic infectious disease caused by Mycobacterium leprae, an acid-fast bacillus that presents a peculiar tropism for peripheral nerves and the skin. The prevalence of leprosy in the world has declined since the introduction of the Multi-Drug Therapy (MDT) recommended by the World Health Organization (WHO)[1]. Leprosy is still a public health problem, especially in Brazil, where the number of new cases detected is high (38.914 cases in 2008)[2]. The predominant route of leprosy transmission is from the contaminated patient’s upper airways to a new host[3], emphasizing the importance of mucosal lesion control. Leprosy-specific oral lesions are generally asymptomatic ulcers or nodules sometimes rich in M. leprae[6,7] resembling nonspecific oral lesions, but they can maintain the focus of infection in endemic areas
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