Figure 1.

Conceptual drawing of the microenvironment of infections in the lung (left) and wound (right). Colonization by bacteria leads to innate immune activation by recognition of pathogen-associated molecular patterns (PAMP) and biofilm-associated molecular patterns (BAMP) by pattern recognition receptors (PRR) and the release of proinflammatory cytokines. Immune cell activation leads to increased O₂ consumption for the respiratory burst which, along with bacterial respiration, leads to lowered O₂ tension. In wounds, bacteria are found as monospecies aggregates separated from each other where different species appear to inhabit different zones of the wound. In lungs of CF patients, bacteria are found intraluminally embedded in thickened sputum. Bacterial interactions occur if signaling molecules reach high enough concentrations to elicit a response. The quorum sensing (QS) system has been shown to be lost or inactive in late infection stages.