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Eine kleine, aber sehr forschungsaktive indische „Gemeinde“ begrüßt die Gesandte ihres Mutterlandes: Am Freitag, 23. März 2012, wird die Leiterin des Generalkonsulats der Republik Indien in Hamburg, Murugesan Subashini, das Helmholtz-Zentrum für Infektionsforschung (HZI) besuchen. Dabei wird sich Subashini nicht nur ein Bild von der biologisch-medizinischen Forschung am Standort Braunschweig machen, sondern auch die indischen Mitarbeiter am HZI treffen. Vorab besucht sie außerdem das Fraunhofer-Institut für Schicht- und Oberflächentechnik IST.

With advancing age, a person's immune system often grows weaker. One reason behind this is the gradual decline of the stem cell population that the body draws on in its ongoing effort to replace old worn-out or damaged immune cells. Now, scientists at the University of Ulm, Germany, in collaboration with the Helmholtz Centre for Infection Research (HZI) in Braunschweig, Germany, have at last identified the mechanism underlying age-related immune function loss. Although it takes place in all cells of the body throughout a person's life, the accumulation of DNA damage in certain blood stem cells activates a gene critical for their differentiation into mature defender cells - a process, which compromises the stem cells' capacity for continuous, lifelong self-renewal, and ultimately responsible for their loss. The researchers' findings are published in the renowned scientific journal Cell and are in fact the current issue's cover story.

In medieval Europe, the Black Death once decimated large parts of the population. Although in Europe no longer a genuine cause for concern, in Africa, South America, and India the Bubonic plague still to this day poses a viable threat to public health. The culprit behind the pandemic is a bacterium of the genus Yersinia. Each year in Germany, the pathogen's slightly less virulent relative is responsible for causing several thousand cases of diarrheal disease – often times with serious consequences. Scientists at the Helmholtz Centre for Infection Research (HZI) in Braunschweig, Germany, working closely with their colleagues at the Ruhr University in Bochum, Germany, have identified a mechanism that enables these bacteria to turn on their weaponry once inside the host. It turns out that Yersinia possesses a built-in molecular thermometer that jump-starts the bacterial pathogenic program at precisely 37 degrees Celsius, which corresponds to normal human body temperature.

Slime-like and near impenetrable are biofilms built by a number of bacterial cells during the course of an infection. Typically, they are composed of long molecular strands called polymers. Many different species of bacteria, among them dangerous pathogens like Pseudomonas and Staphylococcus, use biofilms to shield themselves against the host's immune system attacks and antibiotics' pharmacological mechanism of action. In Germany alone, 100,000 infections annually are related to bacterial biofilms. A joint research initiative by the Helmholtz Centre for Infection Research (HZI) in Braunschweig, Germany, and the TWINCORE, Centre for Experimental and Clinical Infection Research, aims to target bacterial biofilms using Nature's own list of active ingredients.