Trehalose Biosurfactants - Biosurfactants: Research Trends and Applications - page 209

biosurfactants to regulate their surface properties, in order to attach or detach from sur-
faces, according to needs (Ron and Rosenberg 2001). Franzetti et al. (2008) described
that Gordonia cells presented high values of cell surface hydrophobicity in the early
exponential growth, and remained attached to large hydrocarbon drops, so access to the
substrate was by direct contact. During the late exponential phase, cells became hydro-
philic, adhesion to hydrocarbons decreased, and the authors hypothesized that this led
to a change in the mode by which Gordonia cells access the substrate during growth on
hydrocarbons. At the same time, cells excreted extracellular bioemulsifier, allowing the
hydrophilic cells to attach to the hydrophilic outer layer of the emulsified oil droplets.
The present interest in the physiological role of cell-wall trehalose lipids from a
medical point of view has been focused exclusively on mycobacterial cord factors
because of their toxic properties and key role in the pathogenecity of Mycobacteria .
Trehalose 6,6′-dimycolate (TDM) is the most abundant, most granulomagenic, and
most toxic lipid extractable from the surface of virulent Mycobacterium tuberculosis
(Hunter et al. 2006). TDM is the main virulence factor for M. tuberculosis that makes
it resistant to anti-tuberculoses medications. According to Barry et al. (1998), TDM,
together with arabinogalactan mycolate and TMM, forms an integral part of the cell-
wall cytoskeleton, conferring high cell surface hydrophobicity and acid fastness.
Intensive research revealed that mycolic-acid-containing glycolipids, namely TDM
as their best-studied representative, exert a number of immunomodifying effects
(Ryll et al. 2001). They are able to stimulate innate, early adaptive, and both humoral
and cellular adaptive immunity. Most functions can be associated with their ability to
induce a wide range of chemokines (MCP-1, MIP-1alpha, IL-8) and cytokines (e.g.,
IL-12, IFN-gamma, TNF-alpha, IL-4, IL-6, IL-10).
Trehalose lipids from Rhodococcus and related genera showed no growth inhibi-
tion against Gram-negative bacteria and yeasts (Kitamoto et al. 2002). However, tre-
halolipids from R. erythropolis DSMZ 43215 inhibited the conidia germination of the
fungus Glomerella cingulata at a concentration of 300 mg L −1 (Kitamoto et al. 2002).
It was also reported that mice inoculated with TDM emulsion acquired high resis-
tance to intranasal infection by influenza virus (Azuma et al. 1987; Hoq et al. 1997).
Several publications have recently appeared on the biological activities of treha-
lose lipid biosurfactants on phospholipid membranes aiming to gain insight into the
molecular mechanisms of these interactions. Aranda et al. (2007) described molecular
interactions between trehaloselipid and phosphatidylcholine resulting in an alteration
of bilayer stability, and in this respect indicating that trehalose lipid is able to per-
meabilize phospholipid membranes. Ortiz et al. (2008) studied the effect of a purified
from Rhodococcus sp. trehalose lipid on the thermotropic and structural properties of
phosphatidylethanolamine membranes of different chain length and saturation. They
found that the biosurfactant affected the gel-to-liquid crystalline phase transition of
phosphatidylethanolamines, broadening and shifting the transition to lower tempera-
tures. The trehalose lipid did not modify the macroscopic bilayer organization of satu-
rated phosphatidylethanolamines and presented good miscibility both in the gel and
the liquid crystalline phases. The conclusion is that the trehalose lipid incorporates
into the phosphatidylethanolamine bilayers and produces structural perturbations that
might affect the function of the membrane. Similar results were also obtained with
phosphatidylserine membranes (Ortiz et al. 2009). Zaragoza et al. (2009) proposed