SPEAKER
Prof Harald RENZ
Professor and Director, Institute of Laboratory
Medicine and Pathobiochemistry, Molecular
Diagnostics, Philipps University Marburg,
University Hospital Giessen and Marburg GmbH,
Marburg, Germany
HOST:
Department of Infection and Immunity
RESPONSIBLE LIH SCIENTIST:
Prof Dr Markus Ollert (markus.ollert@lih.lu)
www.lih.lu
Supported by:
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THE IMPACT OF THE MICROBIAL EXPOSOME ON ASTHMA AND
ALLERGIC INFLAMMATION
ABSTRACT
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The hygiene hypothesis is currently the leading
concept to explain the dramatic increase in
chronic inflammatory disease including autoimmunities
and allergies. Conversely, several
gram-positive and gram-negative bacteria have
been isolated from rural environmental
communities which provide protection of allergic
asthma.
Overwhelming evidence indicates a strong
impact of environmental microbes on the
programming and the development of (early)
immune responses. Based on clinical and
epidemiological data, a certain exposure of
environmental microbes – particularly of
bacteria – seems to be an important pre-requisite
in order to program immune responses
towards the tolerance default program. This
program on the level of the adaptive immune
responses is necessary and required in order to
prevent unwanted (chronic) inflammatory diseases
which may develop early in life (such as
allergies and asthma) or which may occur even
later in life, such as many autoimmune diseases
at the gut, the brain, or other organs.
The Grand challenge is to define the appropriate
microbial environment on the cellular and
molecular level in order to delineate the underlying
mechanism of microbe-host interaction.
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An important concept in this context. This is the
microbial diversity. Conversely, reduced
diversity is closely linked to several clinical
phenotypes, particularly in early life such as
allergies and asthma. Even more compelling,
reduced diversity precedes the clinical onset of
the disease, suggesting a cause-effect relationship.
This concept implies the loss of (ancient) evolutionary
co-evolved microbial strains and is the result of
changes in lifestyle condition, particularly under
westernized and industrialized environmental
conditions. Therefore, microbial exposure seems to
be a surrogate marker for biodiversity or the loss of
biodiversity, as observed in the above mentioned
living conditions.
The great challenge in this research field is to
delineate the molecular pathomechanism of
gene-environment interactions and the impact of
microbial communities on this complex and intimate
relationship. Only through better
understanding of these mechanisms, we will be
able to define novel and attractive strategies for
the prevention of chronic inflammatory diseases.
Therefore, it is urgently needed to move this
research field towards translational activities. The
next few years will provide a compelling amount of
novel data, which will hopefully improve the understanding
of mechanisms of this important communication
between the host and the microbial
communities.
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