Capsular polysaccharide (CPS)

Capsular polysaccharides (CPS) are complex, high-molecular-weight carbohydrate polymers that form a thick, protective outer layer surrounding the cell wall of Gram-negative bacteria such as Klebsiella pneumoniae and Acinetobacter baumannii. These structures, often designated as K-antigens, are primary virulence factors that enable pathogens to evade the host immune system by masking underlying surface antigens and inhibiting phagocytosis and complement-mediated lysis [1][2]. In K. pneumoniae, specific serotypes like K1 and K2 are strongly associated with hypervirulent phenotypes and invasive diseases like liver abscesses, while in A. baumannii, the capsule is essential for survival during bloodstream infections and resistance to environmental stress [3][4]. Because the CPS is highly immunogenic and surface-exposed, it is a major target for the development of glycoconjugate vaccines, monoclonal antibodies, and novel phage-derived enzymes. These therapies aim to either induce protective antibody responses that enhance bacterial clearance or enzymatically degrade the capsule to restore the efficacy of the host's innate immune defenses [5]. Citations: [1] Wyres, K. L., et al. (2020). Nature Reviews Microbiology. [2] Geisinger, E., & Isberg, R. R. (2015). Nature Reviews Microbiology. [3] Singh, A., et al. (2022). Frontiers in Microbiology. [4] Russo, T. A., & Marr, C. M. (2019). Clinical Microbiology Reviews. [5] Lin, T. L., et al. (2014). Journal of Infectious Diseases.

Other names

K-antigenBacterial capsuleExtracellular polysaccharideK-type antigenSurface polysaccharide

Therapeutic agents targeting capsular polysaccharides typically work through opsonization, where antibodies bind to the CPS to facilitate recognition and ingestion by phagocytes (macrophages and neutrophils). Other mechanisms include the neutralization of the capsule's inhibitory effect on the complement system and the use of phage-derived depolymerase enzymes that specifically degrade the polysaccharide chains, stripping the bacteria of their protective layer and making them vulnerable to host immunity and antibiotics.