Bacterial pathogenesis and interleukin-17: interconnecting mechanisms of immune regulation, host genetics, and microbial virulence that influence severity of infection.
Michelle N ChamounAntje BlumenthalMatthew J SullivanMark A SchembriGlen C UlettPublished in: Critical reviews in microbiology (2018)
Interleukin-17 (IL-17) is a pro-inflammatory cytokine involved in the control of many different disorders, including autoimmune, oncogenic, and diverse infectious diseases. In the context of infectious diseases, IL-17 protects the host against various classes of microorganisms but, intriguingly, can also exacerbate the severity of some infections. The regulation of IL-17 expression stems, in part, from the activity of Interleukin-23 (IL-23), which drives the maturation of different classes of IL-17-producing cells that can alter the course of infection. In this review, we analyze IL-17/IL-23 signalling in bacterial infection, and examine the interconnecting mechanisms that link immune regulation, host genetics, and microbial virulence in the context of bacterial pathogenesis. We consider the roles of IL-17 in both acute and chronic bacterial infections, with a focus on mouse models of human bacterial disease that involve infection of mucosal surfaces in the lungs, urogenital, and gastrointestinal tracts. Polymorphisms in IL-17-encoding genes in humans, which have been associated with heightened host susceptibility to some bacterial pathogens, are discussed. Finally, we examine the implications of IL-17 biology in infectious diseases for the development of novel therapeutic strategies targeted at preventing bacterial infection.
Keyphrases
- infectious diseases
- escherichia coli
- pseudomonas aeruginosa
- staphylococcus aureus
- mouse model
- endothelial cells
- cell death
- poor prognosis
- biofilm formation
- oxidative stress
- liver failure
- cystic fibrosis
- drug delivery
- cell proliferation
- respiratory failure
- extracorporeal membrane oxygenation
- signaling pathway
- cell cycle arrest
- gram negative