The immune system vs.Pseudomonas aeruginosabiofilms

Abstract

Ilya Metchnikoff and Paul Ehrlich were awarded the Nobel price in 1908. Since then, numerous studies have unraveled a multitude of mechanistically different immune responses to intruding microorganisms. However, in the vast majority of these studies, the underlying infectious agents have appeared in the planktonic state. Accordingly, much less is known about the immune responses to the presence of biofilm-based infections (which is probably also due to the relatively short period of time in which the immune response to biofilms has been studied). Nevertheless, more recent in vivo and in vitro studies have revealed both innate as well as adaptive immune responses to biofilms. On the other hand, measures launched by biofilm bacteria to achieve protection against the various immune responses have also been demonstrated. Whether particular immune responses to biofilm infections exist remains to be firmly established. However, because biofilm infections are often persistent (or chronic), an odd situation appears with the simultaneous activation of both arms of the host immune response, neither of which can eliminate the biofilm pathogen, but instead, in synergy, causes collateral tissue damage. Although the present review on the immune system vs. biofilm bacteria is focused on Pseudomonas aeruginosa (mainly because this is the most thoroughly studied), many of the same mechanisms are also seen with biofilm infections generated by other microorganisms.

Nitric oxide production by polymorphonuclear leucocytes in infected cystic fibrosis sputum consumes oxygen

“…Chronic P. aeruginosa lung infection is characterized by the formation of biofilm aggregates surrounded by numerous polymorphonuclear leucocytes (PMNs) in the endobronchial mucus [2]. The biofilm mode of growth protects the bacteria from antibiotics and shields against host defences such as bactericidal defence mechanisms of the activated PMNs [2].…”

“…Chronic P. aeruginosa lung infection is characterized by the formation of biofilm aggregates surrounded by numerous polymorphonuclear leucocytes (PMNs) in the endobronchial mucus [2]. The biofilm mode of growth protects the bacteria from antibiotics and shields against host defences such as bactericidal defence mechanisms of the activated PMNs [2]. Prolonged activation of PMNs in chronic lung infection can cause progressive lung tissue damage by the release of proteolytic enzymes and reactive oxygen species (ROS) [1,3].…”

“…Therefore, we speculate that the activated iNOS and NOX-2 of the PMNs shapes the microenvironment in the infected CF mucus by accelerating O2 depletion and secretion of NO3 − and NO2 − to a level which favours pathogens with anaerobic survival strategies such as denitrification. P. aeruginosa, which tolerates the assaults from activated PMNs by forming biofilm aggregates [2], is a facultative anaerobe capable of denitrification [57]. Therefore, P. aeruginosa is well adaptable to these changes in the lung microenvironment enforced by active PMNs.…”

Bacterial microbiota present in the gallbladder of cattle and antimicrobial resistance of Staphylococcus isolates

“…Salmonella may form permanent colonies and biofilms in gallbladders, triggering the establishment of chronic, asymptomatic carriers (Steenackers et al, 2011). Bacteria in biofilms are generally well protected against environmental stresses, antibiotics, disinfectants and the host immune system (Jensen et al, 2010) and as a consequence, they are extremely difficult to eradicate. Previous studies (Mcdonough et al, 2000;Stoffregen et al, 2004;Reinstein et al, 2006;Jeong et al, 2007) reported isolation of E. coli O157:H7 and Salmonella in gallbladders of cattle and suggested that the organism can reside in these animals' organs.…”

Bead-size directed distribution of Pseudomonas aeruginosa results in distinct inflammatory response in a mouse model of chronic lung infection

“…In fact, both parts of the host immune response contribute to the lung pathophysiology. The constantly recruited polymorphonuclear neutrophil leucocytes (PMNs) contribute by release of exoproteases, reactive oxygen and nitrogen species, and the induced T helper type 2 (Th2)-dominated response contributes by induction of a pronounced antibody response resulting in immune complex disease [1].…”