Pathogens fight back

Opportunistic infections are thought to be caused by pathogens that are generally weaker than other organisms (i.e., have lower virulence) but are able to invade weakened hosts. It has also been suggested that bacteria regulate the expression of virulence factors depending on the chance of successful invasion.1 However, the process whereby bacteria sense changes in the host immune system is only now becoming better understood.

Figure. Pseudomonas aeruginosa Photo by: CDC

Pseudomonas aeruginosa is an opportunistic pathogen that has become a major focus of research owing to its growing resistance to antibiotics. It is a low-virulence organism in immunocompetent hosts, but in immnocompromised patients P. aeruginosa can cause a variety of severe infections. Infections are seen most notably in the respiratory tract, where the pathogen is largely responsible for exacerbations of cystic fibrosis; the skin, where it is the most common cause of burn-related sepsis; and the urinary tract.

New research by Licheng Wu and colleagues reveals that P. aeruginosa may actually use the host's immune system to become more invasive.2 The authors found that interferon-gamma (IFN-γ), a cytokine released by the immune system's T-cells to help clear bacteria, is recognized by P. aeruginosa. They found that when IFN-γ binds to bacteria, virulence factors are activated, thereby providing a countermeasure to the activation of the host immune system.

It has long been known that host immune cells have receptors that recognize bacteria so that the immune response can be activated. It is logical to think that bacteria may in turn have receptors that recognize the immune system for the purpose of monitoring its activation. As the effectiveness of antibiotics wanes, this revelation may help in the development of new ways to suppress bacterial virulence.