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Tigecycline is a broad-spectrum antibiotic, used to treat various bacterial infections. However, the development of resistance to this antibiotic has become a significant concern. Several mechanisms contribute to tigecycline resistance, which can be categorized into three primary categories: efflux pumps, ribosomal protection, and target alteration [1].

1. Efflux pumps: One of the primary mechanisms of tigecycline resistance involves the overexpression of efflux pumps. These pumps are responsible for expelling antibiotics from bacterial cells, thereby reducing the intracellular concentration of the drug. Overexpression of these pumps, often due to genetic mutations, can lead to increased efflux of tigecycline, resulting in decreased susceptibility [1][2].

2. Ribosomal protection: Another mechanism of tigecycline resistance is ribosomal protection. This occurs when bacterial cells produce proteins that can bind to the ribosome, preventing tigecycline from binding to its target site. As a result, the antibiotic's effectiveness is reduced, and bacterial growth can continue [1][2].

3. Target alteration: The third major mechanism of tigecycline resistance is target alteration. This involves genetic mutations that result in changes to the bacterial ribosome, preventing tigecycline from binding effectively. Consequently, the antibiotic's ability to inhibit protein synthesis is compromised, allowing bacterial cells to survive and replicate [1][2].

In summary, the development of tigecycline resistance is a complex process that involves multiple mechanisms, including efflux pumps, ribosomal protection, and target alteration. Understanding these mechanisms is crucial for developing strategies to combat antibiotic resistance and preserve the effectiveness of tigecycline and other antibiotics.

Sources:
[1] Zhanel, G. G., Harding, G. K., Embil, J. A., space,