Agriculture Reference
In-Depth Information
6. Eukaryotic Responses to Bacterial QS Systems
Recent work demonstrates that plants and algae are able to interfere with bacterial QS
communication by secreting compounds that mimic the bacterial-made signals [Tepliski
et
al.
, 2000, Bauer and Robinson, 2002, Mathesius
et al.
, 2003]. The best known mock AHLs
are the structurally analogous halogenated furanones synthesized by the red algae
Delisea
pulchra
(Figure 5), which act blocking communication by binding the bacterial AHL
receptors [Givskov
et al.
, 1996]. Several higher plants (pea, alfalfa) produce compounds that
either activate or inhibit the expression of bacterial genes regulated by QS [Teplitski
et al.
,
2000, Bauer and Mathesius, 2004, Waters and Bassler, 2005, González and Keshavan, 2006].
Bacterial phenotypes controlled by QS are frequently also regulated by additional
environmental signals, ie. oxygen availability, nutrient starvation, iron limitation or catabolite
repression [Newton and Fray, 2004]. Thus, it has been suggested that the plant-produced
mimics are indirectly altering the bacterial QS response, rather than targeting it specifically.
In either case, such compounds may determine the outcome of interactions between higher
plants and a diversity of pathogenic and symbiotic bacteria [Newton and Fray, 2004].
Plants hereby seem able to listen to the bacterial language, and possibly also respond
directly to AHLs-based signaling systems of either beneficial or harmful bacteria. This later
hypothesis is also supported by data on the influence of physiologically relevant
concentrations of AHLs on proteome profiles of
Medicago truncatula
roots, showing that
AHLs induce the accumulation of root proteins involved in host defense responses [Mathesius
et al
. 2003]. Elicitation of defense responses by AHLs is also proven in tomato and bean
plants [Bauer and Mathesius, 2004]. Finally, there is some evidence of plant produced
compounds able to interact with bacterial communication mediated by AI-2 [Bauer and
Mathesius, 2004].
Other responses of eukaryotic organisms to the AHL-based bacterial QS systems have
been described. Motile zoospores of the sea green algae
Enteromorpha
preferentially attach to
AHL-producing bacterial biofilms, due to AHLs acting as chemo-attractants [Joint
et al.,
2002]. Bacterial AHLs elicit several responses in animals, such as immunomodulatory and
haemodynamic effects in rats, inhibition of muscle contraction in pigs, and accelerated
apoptosis in macrophages and neutrophils [Bauer and Mathesius, 2004].
Recent findings have given evidence of the ability of human cells to hamper bacterial QS
by inactivation of the signal molecules.
Pseudomonas aeruginosa
is an opportunistic
pathogen that causes infections mostly in immune compromised patients. Human respiratory
epithelia have the capacity to inactivate the
P. aeruginosa
quorum-sensing signal 3-oxo-C
12
-
HSL, by means of a membrane-associated enzymatic mechanism [Chun
et al.
, 2004]. This
capacity functions in some but not all mammalian cells [Hastings, 2004]. The ability
of
epithelial cells to inactivate 3-oxo-C
12
-HSL may confer host
protection against
P. aeruginosa
infections and could be exploited as a therapeutic target. Human hormones epinephrine and
norepinephrine also interfere with the QS system of enterohemorrhagic
Escherichia coli
[Sperandio
et al.
, 2003]. The interference on bacterial QS mechanisms by plants and animals
acting as hosts of bacterial pathogens is hypothesized as part of the multiple defense strategies
developed by eukaryotes to avoid bacterial infections.
