Bacteria and host: what does this mean for sepsis bottleneck?

Azzah S Alharbi, Raghad Hassan Sanyi, Esam I Azhar

Figure 1. Schematic presentation of parallel dynamics of selective pressures experienced by pathogens, which produce so-called bottlenecks, and the quality of the systemic inflammatory response. Recent experimental evidence has led to the development of a new sepsis model, challenging the traditional sepsis inflammatory concept in which an initial hyper-inflammatory response is followed by an immunosuppressive phase. This new sepsis model suggests the existence of a mixed inflammatory (heterogeneous) response in the initial phase of septicaemia.[69] The scale of the inflammatory response in sepsis can create a hostile environment for pathogens, applying strong selection pressure on the bacterial population (inoculum). This pressure may continuously result in a “bottleneck” effect, reducing the overall diversity of the bacterial population by allowing only specific clones with traits that enable them to survive immune assault to persist and proliferate. These surviving clones often possess adaptations, such as increased virulence factors or resistance to host defenses, which provide them with a survival advantage against immune system attack. Each pathogen is depicted as a colored sphere, with different colors representing distinct markers. The pro-inflammatory response is represented by the red line and red gradient, whereas the anti-inflammatory response is represented by the blue line and blue gradient.