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Pathog Dis. 2016 Apr;74(3). pii: ftw004. doi: 10.1093/femspd/ftw004. Epub 2016 Jan 17.

Sensing developing biofilms: the bitter receptor T2R38 on myeloid cells.

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Institute for Pathology, Heidelberg University, Im Neuenheimer Feld 224, 69120 Heidelberg, Germany.
Center for Orthopaedics, Trauma Surgery and Spinal Cord Injury, Heidelberg University Hospital Schlierbacher Landstrasse 200a, 69118 Heidelberg, Germany
Institute for Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120 Heidelberg, Germany.


Quorum-sensing molecules, also known as autoinducer, are essential for bacterial biofilm formation. Our focus is on N-(3-oxododecanoyl)-L-homoserine lactone (AHL-12), because it is also known as an 'interkingdom signalling molecule', which means that it also interacts with mammalian cells. AHL-12 activates defence-relevant functions of phagocytic cells, including enhancement of phagocytosis, increased expression of adhesion receptors and induction of chemotaxis. This leads to the hypothesis that early recognition of developing biofilms might be the key to a successful host defence against biofilm infection. In that context we studied activation of phagocytic cells by AHL-12, and found that phagocytes are activated via a rather specialized receptor that was not previously described on myeloid cells, the bitter taste receptor T2R38. Taste receptors are commonly associated with cells of the gustatory system. The extragustatory expression, however, suggests an additional role, namely the sensing of the onset of bacterial biofilm infection.


AHL-12; T2R38; biofilm; bitter receptor; innate immune response; lipid droplets

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