Klebsiella pneumoniae: Going on the Offense with a Strong Defense

Abstract

SUMMARYKlebsiella pneumoniaecauses a wide range of infections, including pneumonias, urinary tract infections, bacteremias, and liver abscesses. Historically,K. pneumoniaehas caused serious infection primarily in immunocompromised individuals, but the recent emergence and spread of hypervirulent strains have broadened the number of people susceptible to infections to include those who are healthy and immunosufficient. Furthermore,K. pneumoniaestrains have become increasingly resistant to antibiotics, rendering infection by these strains very challenging to treat. The emergence of hypervirulent and antibiotic-resistant strains has driven a number of recent studies. Work has described the worldwide spread of one drug-resistant strain and a host defense axis, interleukin-17 (IL-17), that is important for controlling infection. Four factors, capsule, lipopolysaccharide, fimbriae, and siderophores, have been well studied and are important for virulence in at least one infection model. Several other factors have been less well characterized but are also important in at least one infection model. However, there is a significant amount of heterogeneity inK. pneumoniaestrains, and not every factor plays the same critical role in all virulentKlebsiellastrains. Recent studies have identified additionalK. pneumoniaevirulence factors and led to more insights about factors important for the growth of this pathogen at a variety of tissue sites. Many of these genes encode proteins that function in metabolism and the regulation of transcription. However, much work is left to be done in characterizing these newly discovered factors, understanding how infections differ between healthy and immunocompromised patients, and identifying attractive bacterial or host targets for treating these infections.

Розвиток Імунної Відповіді При Стафілококовій Пневмонії (Частина 3)

“…Известно, что IL-10 ингибирует экспрессию антигенов II класса глав-ного комплекса гистосовместимости и костимули-рующих молекул АРС, что приводит к снижению активации Т-клеток. В отличие от ингибирующего влияния на клеточный иммунитет на гуморальное звено IL-10 оказывает стимулирующее влияние: он активирует пролиферацию B-клеток и усиливает синтез иммуноглобулинов [73,80,83,99].…”

The threat of carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-HvKP)

“…Antibiotic resistance of cKP is significantly high worldwide [3], but HvKP is rarely resistant to antibiotics, except for an intrinsic resistance to ampicillin [6,10]. However, recent many reports have shown the emergence of antibiotic-resistant HvKP strains [6].…”

The contribution of capsule polysaccharide genes to virulence of Klebsiella pneumoniae

“…In the bacterium, the capsule confers resistance against the bactericidal activity of antimicrobial peptides, complement, and phagocytes. 1 In addition, the capsule averts fulminant activation of the immune response. 4 Acapsular K. pneumoniae strains are markedly less virulent than isogenic encapsulated strains in mouse models, 5,6 and the strains that produce a capsule conferring a hypermucoviscous phenotype become HV.…”

“…K. pneumoniae can spread from colonizing sites to other tissues, leading to urinary tract infections, pneumonia, and other infections in humans. 1 Recently, concerns have arisen due to the emergence and dissemination of hypervirulent (HV) or antibiotic resistant strains. 2,3 To date, several K. pneumoniae virulence factors have been identified: the capsule, lipopolysaccharide, siderophores, and fimbriae (also known as pili).…”

“…2,3 To date, several K. pneumoniae virulence factors have been identified: the capsule, lipopolysaccharide, siderophores, and fimbriae (also known as pili). 1 Of these, the capsule, which is synthesized by gene products from the capsular polysaccharide synthesis (cps) locus, is the most thoroughly studied virulence factor for K. pneumoniae. In the bacterium, the capsule confers resistance against the bactericidal activity of antimicrobial peptides, complement, and phagocytes.…”