Tuberculosis: From Pathogenesis to Targeted Therapies
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 7525
Special Issue Editor
Special Issue Information
Dear Colleagues,
Most bacterial infections can quickly be cured by antibiotic monotherapy. In contrast, drug-sensitive tuberculosis (TB) must be treated with a combination of four antibiotics over 6 months. This lengthy, multidrug regimen often confounds compliance, leading to treatment failure, recurrence of TB, and the emergence of antibiotic-resistant mycobacteria. The goal of current TB research is, therefore, not only the development of new antibiotics and identification of novel antibiotic targets but also to find therapies that shorten treatment time. One reason for the need for such a long-term therapy is the development of centrally necrotizing granulomas in TB patients. This hallmark of TB pathogenesis represents not only a physical barrier, which often hinders the efficient penetration of antibiotics into the necrotic lesions. Additionally, within these types of granulomas particular conditions prevail, such as permissive cells, devascularization of the necrotic center, physicochemical peculiarities of the caseous content, and the presence of extracellular, quiescent mycobacteria with special metabolic adaptations that all pose a challenge to the efficacy of compounds. Hence, new drugs and regimens for the therapy of TB must consider the pathogenesis of this complex disease, ensuring that compounds can reach their target and act more effectively within the habitat of centrally necrotizing granulomas. This Special Issue aims to cover new research on the pathogenesis of TB in terms of therapy and novel compounds, as well as present host-directed strategies that mediate better and faster antibiotic treatment through modulation of the pathology.
Dr. Christoph Hölscher
Guest Editor
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Keywords
- tuberculosis
- therapy
- granuloma
- antibiotics
- host-directed
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