The adhesion of bacteria to host cells is always the first and one of the decisive steps in the development of infectious diseases. The purpose of this adhesion by infectious pathogens is first to colonize the host organism (i.e. the human body) and then to initiate an infection which in the worst case may end in the death. A precise understanding of bacterial adhesion to host cells is essential to find therapeutic alternatives that block this critical interaction at the earliest possible stage of an infection.
Critical interaction with the human protein fibronectin
Together with other researchers, scientists from Frankfurt University Hospital and Goethe University Frankfurt have now explained the exact mechanism of bacterial adhesion using the human pathogenic bacterium. Bartonella henselae. This pathogen causes “cat-scratch disease”, a disease transmitted from animals to humans. In an international collaborative project led by the Frankfurt research group led by Professor Volkhard Kempf, the mechanism of bacterial adhesion has been deciphered using a combination of in vitro adhesion assays and high-throughput proteomics . Proteomics is the study of all the proteins present in a cell or a complex organism.
Scientists have shed light on a key mechanism: bacterial adhesion to host cells can be attributed to the interaction of a certain class of adhesins – called “trimeric autotransport adhesins” – with fibronectin, a protein often present in human tissues. . Adhesins are components on the surface of bacteria that allow the pathogen to adhere to the biological structures of the host. Homologs of the adhesin identified here as critical are also present in many other bacteria pathogenic to humans, such as the multidrug-resistant bacterium Acinetobacter baumanniiwhich the World Health Organization (WHO) has classified as the top priority for research into new antibiotics.
State-of-the-art protein analyzes were used to visualize the exact points of protein interaction. Moreover, it was possible to show that the experimental blocking of these processes almost entirely prevents bacterial adhesion. Therapeutic approaches aimed at preventing bacterial adhesion in this way could represent a promising treatment alternative as a new class of antibiotics (so-called “anti-ligands”) in the constantly growing field of multi-resistant bacteria.
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