Cell Host & Microbe,
Journal Year:
2016,
Volume and Issue:
19(3), P. 311 - 322
Published: March 1, 2016
Human
immunodeficiency
virus
(HIV)
infection
is
associated
with
increased
intestinal
translocation
of
microbial
products
and
enteropathy
as
well
alterations
in
gut
bacterial
communities.
However,
whether
the
enteric
virome
contributes
to
this
resulting
remains
unknown.
We
characterized
microbiome
a
cohort
Ugandan
patients,
including
HIV-uninfected
or
HIV-infected
subjects
those
either
treated
anti-retroviral
therapy
(ART)
untreated.
Low
peripheral
CD4
T
cell
counts
were
an
expansion
adenovirus
sequences
increase
was
independent
ART
treatment.
Additionally,
patients
lower
exhibited
reduced
phylogenetic
diversity
richness
specific
bacteria
showing
differential
abundance,
increases
Enterobacteriaceae,
which
have
been
inflammation.
Thus,
progressive
HIV
microbiome,
may
contribute
AIDS-associated
disease
progression.
Annual Review of Immunology,
Journal Year:
2020,
Volume and Issue:
38(1), P. 23 - 48
Published: April 26, 2020
The
gastrointestinal
tract
harbors
numerous
commensal
bacteria,
referred
to
as
the
microbiota,
that
benefit
host
health
by
digesting
dietary
components
and
eliminating
pathogens.
intestinal
microbiota
maintains
epithelial
barrier
integrity
shapes
mucosal
immune
system,
balancing
defense
oral
tolerance
with
microbial
metabolites,
components,
attachment
cells.
To
avoid
aberrant
responses,
cells
segregate
from
constructing
chemical
physical
barriers,
leading
establishment
of
host-commensal
mutualism.
Furthermore,
participate
in
maintenance
a
healthy
community
reinforce
functions.
Perturbations
composition
are
commonly
observed
patients
autoimmune
diseases
chronic
inflammatory
disorders.
An
understanding
intimate
interactions
between
cells,
crucial
for
homeostasis
might
promote
advances
diagnostic
therapeutic
approaches
various
diseases.
Frontiers in Microbiology,
Journal Year:
2018,
Volume and Issue:
9
Published: Sept. 25, 2018
In
the
twenty
first
century,
changing
epidemiology
of
inflammatory
bowel
disease
(IBD)
globally
with
increasing
incidence
across
many
countries
relates
to
altered
gut
microbiota,
due
a
combinatorial
effect
environmental
factors,
human
immune
responses
and
genetics.
IBD
is
gastrointestinal
associated
dysbiosis,
characterized
by
changes
in
microbial
communities
that
include
an
expansion
facultative
anaerobic
bacteria
family
Enterobacteriaceae.
Advances
high-throughput
sequencing
enable
us
entangle
microbiota
health
beyond
bacterial
including
mycobiota,
virobiota
helminthes.
Caudovirales
(viruses)
Basidiomycota,
Ascomycota
C.albicans
(fungi)
are
revealed
be
increased
IBD.
The
deconvolution
lays
basis
for
unveiling
roles
these
various
components
pathogenesis
being
conductive
instructing
on
future
diagnosis
therapeutics.
Here
we
comprehensively
elucidate
alterations
IBD,
discuss
diets
relation
illustrate
potential
manipulation
therapeutic
strategy
antibiotics,
probiotics,
prebiotics
fecal
transplantation
will
benefit
effective
application
precision
microbiome
Science,
Journal Year:
2019,
Volume and Issue:
365(6452)
Published: Aug. 1, 2019
Laboratory
mouse
studies
are
paramount
for
understanding
basic
biological
phenomena
but
also
have
limitations.
These
include
conflicting
results
caused
by
divergent
microbiota
and
limited
translational
research
value.
To
address
both
shortcomings,
we
transferred
C57BL/6
embryos
into
wild
mice,
creating
"wildlings."
mice
a
natural
pathogens
at
all
body
sites
the
tractable
genetics
of
mice.
The
bacterial
microbiome,
mycobiome,
virome
wildlings
affect
immune
landscape
multiple
organs.
Their
gut
outcompete
laboratory
demonstrate
resilience
to
environmental
challenges.
Wildlings,
not
conventional
phenocopied
human
responses
in
two
preclinical
studies.
A
combined
microbiota-
pathogen-based
model
may
enhance
reproducibility
biomedical
increase
bench-to-bedside
safety
success
immunological
Science,
Journal Year:
2017,
Volume and Issue:
357(6350), P. 498 - 502
Published: Aug. 3, 2017
The
microbiota
is
known
to
modulate
the
host
response
influenza
infection
through
as-yet-unclear
mechanisms.
We
hypothesized
that
components
of
exert
effects
type
I
interferon
(IFN),
a
hypothesis
supported
by
analysis
in
gain-of-function
genetic
mouse
model.
Here
we
show
microbially
associated
metabolite,
desaminotyrosine
(DAT),
protects
from
augmentation
IFN
signaling
and
diminution
lung
immunopathology.
A
specific
human-associated
gut
microbe,
Clostridium
orbiscindens,
produced
DAT
rescued
antibiotic-treated
influenza-infected
mice.
protected
priming
amplification
loop
signaling.
These
findings
enteric
have
distal
on
responses
lethal
infections
modulation
IFN.
