Abstract
Mycobacterium avium is a human pathogen that causes infection in immunocompetent as well as immunocompromised patients. Infection is acquired both by the respiratory and gastrointestinal routes, and bacterial invasion of mucosal epithelial cells is characteristic. M. avium crosses the mucosal barrier without triggering substantial inflammatory response. Once in the intestinal submucosa or in the alveolar space M. avium infects macrophages. Intracellular bacteria block the production of cytokines involved in the host response against the infection, such as TNF-α and IL-12, and suppress antigen presentation by the macrophage. Innate response against the infection is effective to certain extent but the ability of the bacterium to remain “silent” for a period of time prevents neutrophil and NK cells from effectively controlling the establishing of the infection. CD4+ T cells as well as CD8+ T cells are activated, although only CD4+ T cells appear to be effective in inducing anti-M. avium activity in macrophages. M. avium-specific CD8+ T cells undergo apoptosis early in the infection. Therefore, the immune mechanisms of the host and bacterial strategies for survival are complex and fascinating.
Keywords: Cytokines, macrophages, immunocompetent
Current Pharmaceutical Design
Title: Role of Type I Cytokines in Host Defense Against Mycobacterium avium Infection
Volume: 9 Issue: 1
Author(s): Lia Danelishvilli and Luiz E. Bermudez
Affiliation:
Keywords: Cytokines, macrophages, immunocompetent
Abstract: Mycobacterium avium is a human pathogen that causes infection in immunocompetent as well as immunocompromised patients. Infection is acquired both by the respiratory and gastrointestinal routes, and bacterial invasion of mucosal epithelial cells is characteristic. M. avium crosses the mucosal barrier without triggering substantial inflammatory response. Once in the intestinal submucosa or in the alveolar space M. avium infects macrophages. Intracellular bacteria block the production of cytokines involved in the host response against the infection, such as TNF-α and IL-12, and suppress antigen presentation by the macrophage. Innate response against the infection is effective to certain extent but the ability of the bacterium to remain “silent” for a period of time prevents neutrophil and NK cells from effectively controlling the establishing of the infection. CD4+ T cells as well as CD8+ T cells are activated, although only CD4+ T cells appear to be effective in inducing anti-M. avium activity in macrophages. M. avium-specific CD8+ T cells undergo apoptosis early in the infection. Therefore, the immune mechanisms of the host and bacterial strategies for survival are complex and fascinating.
Export Options
About this article
Cite this article as:
Danelishvilli Lia and Bermudez E. Luiz, Role of Type I Cytokines in Host Defense Against Mycobacterium avium Infection, Current Pharmaceutical Design 2003; 9 (1) . https://dx.doi.org/10.2174/1381612033392369
DOI https://dx.doi.org/10.2174/1381612033392369 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
The Antioxidants and Pro-Antioxidants Network: An Overview
Current Pharmaceutical Design Imaging Reporters and Multimodal Molecular Bio-Imaging: A Database of Available Probes for Multi-Modality Bio-Imaging of Reporter Gene Expression
Recent Patents on Medical Imaging Nanoemulsions for Skin Targeting: Present Status and Future Prospects
Drug Delivery Letters Immunosuppressive Drugs in HIV Disease
Current Topics in Medicinal Chemistry Importance of Propellants and Excipients in Pharmaceutical Topical Aerosol
Current Drug Delivery Apoptotic Pathways in the Pathogenesis of Pemphigus: Targets for New Therapies
Current Pharmaceutical Biotechnology A Systematic Review of Randomized Controlled Trials Examining the Nephroprotective Properties of Antihypertensive Medications
Current Hypertension Reviews Dysregulated Interleukin -33/ST2 Pathway Perpetuates Chronic Inflammation in Hashimoto’s Thyroiditis
Endocrine, Metabolic & Immune Disorders - Drug Targets Apolipoprotein Mimetic Peptides as Modulators of Lipoprotein Function
Protein & Peptide Letters Function and Regulation of Tumor Necrosis Factor Receptor Type 2
Current Medicinal Chemistry Protein and Antibody Engineering: Suppressing Degranulation of the Mast Cells and Type I Hypersensitivity Reaction
Current Protein & Peptide Science Cerebrospinal Fluid Proteomes: From Neural Development to Neurodegenerative Diseases
Current Proteomics Finding Recurrent Copy Number Alteration Regions: A Review of Methods
Current Bioinformatics CDC25 Phosphatase Inhibitors: An Update
Mini-Reviews in Medicinal Chemistry Control of Protein Synthesis in Malignant Transformation - the Role of eIF4E and the eIF4E Binding Proteins in the Regulation of Apoptosis
Current Cancer Therapy Reviews Pandemic Influenza: Preventing the Emergence of Novel Strains and Countermeasures to Ameliorate its Effects
Infectious Disorders - Drug Targets Macrolactins: Antitumor Antibiotics as Marine Drug Lead
Current Organic Chemistry Advances in Hydrogels Applied to Degenerative Diseases
Current Pharmaceutical Design Chemical and Pharmacological Aspects of Heteroaryl-Nitrones
Current Medicinal Chemistry T Cell Tuning for Tumour Therapy: Enhancing Effector Function and Memory Potential of Therapeutic T cells
Current Gene Therapy