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Printable Handouts
Navigable Slide Index
- Introduction
- Conflict of interest
- Immune tolerance and breakdown of tolerance to ingested antigens
- Distribution of bacterial phyla at different anatomical sites
- The composition of the bacterial, fungal, and viral microbiota at distinct body sites
- Microbes prime immune cells in utero
- Caesarean section is an important risk factor
- Development of barrier microbiome homeostasis
- Abrupt shifts in commensal microbiota
- Development of gut microbial communities
- Postnatal risk factors for the development of allergy and asthma
- Additive effect of maternal and infant risk factors on childhood asthma
- Short-chain fatty acids (SCFA)
- Prebiotics
- SCFA associated with asthma protection
- Postbiotics
- Diet – microbes – immune modulation
- Depleted microbial diversity and increased chronic inflammation
- Microbial metacommunity in early life
- Impact on asthma development and/or exacerbation
- Acinetobacter lwoffii
- Repeated intranasal Acinetobacter Iwoffii administration triggers inflammatory response
- Study results
- Environmental bacteria regulate the mucosal – microbial – immune interface
- The concept of diversity
- Biodiversity
- Biodiversity hypothesis
- Probiotics
- Main bacterial genera isolated from human milk
- The world of carbohydrate prebiotics
- Mechanisms by which prebiotics influence the gut microbiota
- Multiple physiological effects of HMOs
- Microbiome and allergy/asthma - 2023
Topics Covered
- Immune tolerance and breakdown of tolerance
- Microbial signature is influenced by maternal, lifestyle, and environmental factors
- Postnatal risk factors for the development of allergy and asthma
- Short-chain fatty acids (SCFA)
- Prebiotics, probiotics, and postbiotics
- Diet, microbes, and immune modulation
- Depleted microbial diversity and increased chronic inflammation
Links
Series:
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Therapeutic Areas:
External Links
Talk Citation
Renz, H. (2024, January 31). The microbiome and allergic diseases [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 21, 2024, from https://doi.org/10.69645/XHMT9092.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Renz has received support for his research from the following organisations: DFG, BMBF, EU, Land Hessen, DAAD, ALK, Stiftung Pathobiochemie, GIZ. Prof. Renz has also received honorariums from Allergopharma, Novartis, ThermoFisher, Danone, Bencard, and Stallergenes, and he is also a consultant and co-founder of Sterna-biologicals. Additionally, Prof. Renz is an Associate Editor for the Journal of Allergy and Clinical Immunology (JACI).
Other Talks in the Series: Allergy - From Basics to Clinic
Transcript
Please wait while the transcript is being prepared...
0:00
Hello everybody. My
name is Harald Renz,
and I'm from the Institute
of Laboratory Medicine at
the Philipps University
of Marburg in Germany.
I'm going to talk about
the microbiome and
allergic diseases.
0:17
Here are my conflict
of interest.
Particularly, I would like to
focus on my editorial activities
as Associate Editor of
the Journal of Allergy
and Clinical Immunology.
0:32
When we are talking
about the role
and the function
of a microbiome,
it is very important to connect
the microbiome with
our immune system.
Our normal default program of
the immune system is shown on
the left-hand side
of this slide,
and that is the development of
clinical and
immunological tolerance.
The development of tolerance
requires antigen contact.
It's an active process
of the immune system.
It is closely related
to the development of
regulatory T cells and
other cell types of the
adaptive immune system,
which are secreting
interleukin 10
and TGF-beta and
other cytokines.
However, if this
default program cannot
develop or is interrupted
or is disturbed,
then this gives room and
space for the development
of pathologic pathogenic,
chronic inflammation.
Again, this is inflammation
controlled and directed
by T lymphocytes.
But in this case, these are
different effector
T-cell responses.
We term them in the most
simple classification
as T helper 1 or T helper 2
type inflammatory responses.
You see here on the
right-hand side of this slide
an example of such pathogenic
inflammatory response.
In this case, it is T helper 2
type inflammatory
reaction, which
is mainly orchestrated by
the cytokines secreted by
these T helper 2 cells.
These T helper 2 cells
are instructed by
epithelial cells which have
encountered pathogens,
bacteria, microbes,
but also allergens.
Now comes the microbiome
into this picture.
The microbiome is
actually the exposure,
the qualitative and
quantitative composition
of the exposure of
the epithelial barrier of
the epithelial layers to
environmental microbes
and microbes which
have seeded here in
these cell spaces.
These microbes interact very
closely with our
epithelial barrier,
but also with the immune
cells directly themselves.
This close and intimate
interaction actually is
responsible for the education
and for the training
of the immune system.
With the right microbes
at the right time,
at the right place,
we are able to develop
a tolerogenic type
of immune response.
But if we have
wrong microbes at the wrong
time in the wrong place,
this opens way to
the development of
pathogenic inflammation.
Now it is very
important to better
understand the mechanisms
underlying this paradigm.
Here we have made some
substantial progress
over the last few years,
which I would like to share with
you throughout my presentation.
On the next slide, you
see the distribution
of this microbiome in our body.