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A recipe for a nasty bug

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  • A recipe for a nasty bug

    Evolution has taught microbes seeking accommodation in humans how to cheat us. An infection biology research programme studies the tricks our tormentors know.

    Professor, immunologist Seppo Meri believes that he will later in life develop latent macular degeneration in his eyes. Unfortunately it is partly hereditary. Yet his colleagues, if anyone, may come up with a treatment for the disease that dots his visual field before the professor reaches the milestone of 65 years which is critical for the disease.

    For a non-expert, the connection between age-related macular degeneration and the human immune system is somewhat unclear. Defence against microbes and dots in the visual field – what can they possibly have in common?

    “Well, it did surprise the researchers,” Meri says. Microbes have gradually been detected in the background of other diseases as well, such as gastric ulcers, arthritis and arteriosclerosis. In the case of some other diseases, those nasty infectious agents skulking in the body are still being sought. Professor Meri takes diabetes as an example. “The destruction of pancreatic islet cells appears to be connected to inflammations caused by enteroviruses.” However, it can take years before the symptoms of cell destruction and diabetes show up.

    What about the black dots in the visual field?

    “Besides eliminating intruders, our immune system has many other tasks.

    One of the biggest is to dispose of the waste produced by the body. Debris such as damaged cells must be removed to prevent inflammation,” Meri says. “Age-related macular degeneration is related to deposits of retinal pigment in the eye that the immune system cannot eliminate. The cell is not properly cleaned, which is partly hereditary.”

    Thick-skinned bacteria

    Professor Meri studies inflammatory diseases and the immune system at the Haartman Institute. He is also the leader of the infection biology research programme investigating the same topic. “Infections and the immune system are now studied from the viewpoint of microbes in particular,” Meri says.

    The research teams in the programme study their respective microbes but work at the same site. They all want to know what turns a germ into a pathogen. In other words: what helps a microbe slip past the immune system?

    While the virulence factors of microbes – their capacity for causing disease – vary, some generalisations can be made. “First of all, the microbe must have an adhesive protein on its surface to stick to human tissue,” Meri says. “This adhesiveness largely explains the species-specific nature of microbes.” A micro-organism that gets a hold of the receptors in human cells often cannot adhere to the cells of other animals.

    Secondly, a virus, bacterium or parasite needs the tools to invade the human body and avoid its immunologic defence mechanisms. “The success of many bacteria is based on their ability to disguise themselves or otherwise elude the killer cells in the human body,” Meri says.

    Then there are viruses and some bacteria and protozoa that have discovered a way to survive inside a phagocyte. They can avoid being driven into the lysosomes of cells where their protecting membrane gets destroyed. Some of them survive the various toxins inside the lysosome; the thick-skinned mycobacterium tuberculosis thrives in the phagocyte.

    The third item in the microbes’ survival kit is the ability to reproduce. A favourable nest site must be found in places such as human skin, a joint, a kidney or the brain.

    If the intruder doesn’t multiply a millionfold, it can be rather harmless and lead its life at leisure in human tissue,” Meri says, “provided that it does not excrete any hazardous toxins, of course.”

    The rule of thumb is that the worse the pathogen, the more it contains avoidance mechanisms to cheat the immune system. The same applies to us humans: our immune system has many defence mech-anisms, some of which overlap. If one mechanism fails, others will replace it.

    Headline diseases

    The team of virologists headed by Professor Klaus Hedman has discovered a new way to determine the age of infections. For example, it is necessary to know the history of rubella antibodies found in a pregnant woman. The antibodies can be harmless remnants of an old disease or a sign of an acute infection that can have devastating consequences for the foetus.

    Hedman and his team realised that, when studying a rubella infection, one has to pay attention to the strength of the binding between the antibodies and the microbe. While antibodies are looser in a fresh infection, tightly bound or high-avid antibodies are a sign of a more advanced disease.

    Meri’s team has used the Borrelia bacterium to study the coexistence of microbes with people. Their goal is to understand the ways in which the bacterium evades our immune system. The team’s cooperation partners have studied diagnostics, and the result of their work will also benefit more than just researchers. They have developed tests for the identification of infections caused by the three different Borreliae that torment people. “Our Swedish partners have been working hard this summer picking ticks from bird nets for bacteria cultivation. Bird ticks carry the bacterium that causes Lyme disease, the borreliosis that affects the central nervous system,” Meri says.

    Other Borreliae are found in rodent and deer ticks, for instance, which only bite other animals, not people.”

    Borreliosis is topical issue in the Finnish media every summer, and the infection biology research programme also has many other interesting topics. While zoonoses such as avian flu usually make the biggest headlines, epidemics often lead the media also to discuss topics such as MRSA and other hospital infections.

    A two-front war

    The human immune defence system is a two-front war: the immediate response is provided by natural or innate immunity and the specific response by learned or adaptive immunity.

    The innate immune system provides an immediate and lethally effective response but a rather rough identification of pathogens and damaged structures. If there is an intruder in the body, the immune system triggers an inflammation that invites the police and fire brigade of the body to the site.

    Familiar from lab tests, CRP or the C-reactive protein is a marker of inflammation that identifies tissue damage; leukocytes or white blood cells devour intruding microbes; and dendrite cells swimming in the lymph report any enemy sightings to the immune cells in the lymph nodes.

    The backbone of innate immunity is the complement system: over 30 different proteins that protect the body as a biochemical cascade, a series of chemical reactions. The body has sensors that detect foreign genetic material, recognise certain microbial tails or mark useless cells as waste.

    Professor Seppo Meri’s research team has developed diagnostic methods to detect the lack of any protective protein in the complement system.

    Malfunctions in the system manifest themselves in various conditions such as susceptibility to infection, meningitis, macular degeneration, oedema and haemolysis.

    The adaptive immune system with its antibodies and lymphocytes is based on immunological memory where the intruder’s features are saved from the previous attack almost to the atom. Specific antibodies are tailored for each pathogen.

    One of the main control centres of the adaptive immune system is the cell school located in the thymus where young lymphocytes or T cells are trained. Training ensures that the T cells know their enemies but do not become crooked policemen who attack the body’s own cells and cause autoimmune disease.

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    "The next major advancement in the health of American people will be determined by what the individual is willing to do for himself"-- John Knowles, Former President of the Rockefeller Foundation
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