Sports and Immunity, from the recreational to the elite athlete
Richard Baskerville,
No information about this author
L M Castell,
No information about this author
Stéphane Bermon
No information about this author
et al.
Infectious Diseases Now,
Journal Year:
2024,
Volume and Issue:
54(4), P. 104893 - 104893
Published: March 24, 2024
The
pivotal
role
of
the
immune
system
in
physical
activity
is
well-established.
While
interactions
are
complex,
they
tend
to
constitute
discrete
responses.
Moderate
intensity
exercise
causes
leukocytosis
with
a
mild
anti-inflammatory
cytokine
profile
and
immunoenhancement.
Above
threshold
intensity,
lactate-mediated
IL-6
release
proinflammatory
state
followed
by
depressed
inflammatory
state,
which
stimulates
adaptation
longer
term
cardiometabolic
enhancement.
Exercise-related
responses
modulated
sex,
age
immunonutrition.
At
all
ability
levels,
these
factors
collectively
affect
balance
between
enhancement
or
overload
dysfunction.
Excessive
training,
mental
stress
insufficient
recovery
risks
cell
exhaustion
hypothalamic
pituitary
axis
(HPA)
causing
immunodepression
negative
impacts
on
performance
general
health.
Participation
sport
provides
additional
benefits
terms
ensuring
regularity,
social
inclusion,
well-being
healthier
life
choices
diet
reduced
smoking
alcohol,
thereby
consolidating
healthy
lifestyles
Significant
differences
exist
recreational
professional
athletes
inherent
characteristics,
training
resilience
stresses
arising
from
competition
schedules,
travel-related
infections
stress.
Exercise
immunology
examines
central
immunity
physiology
straddles
multiple
disciplines
ranging
neuroendocrinology
nutrition
genetics,
aim
guiding
train
optimally
safely.
This
review
brief
outline
main
exercise,
some
influencing
factors,
current
guidance
maintaining
Language: Английский
Studying Cellular Senescence Using the Model Organism Drosophila melanogaster
Methods in molecular biology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 281 - 299
Published: Jan. 1, 2025
Language: Английский
Leptina: descripción de su intrigante biología. Una revisión. Parte I
Cardiovascular and Metabolic Science,
Journal Year:
2025,
Volume and Issue:
36(1), P. 58 - 69
Published: Jan. 1, 2025
Maternal Iron Deficiency Modulates Antioxidant Status and Longevity in a Sex-Dependent Manner in Drosophila melanogaster
Saudat Faruk,
No information about this author
Kasimu Ibrahim Ghandi,
No information about this author
Abdullahi Y. Abbas
No information about this author
et al.
Research Square (Research Square),
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 16, 2025
Abstract
Background:
Maternal
iron
deficiency
(ID)
disrupts
both
maternal
and
offspring
health
by
impairing
status
antioxidant
defenses.
This
study
examines
the
intergenerational
effects
of
ID
rapamycin
intervention
on
Drosophila
melanogaster.
Rapamycin
is
known
for
promoting
autophagy,
longevity,
activity.
Method:
Female
flies
(F0)
were
subjected
to
an
iron-deficient
diet
14
days,
followed
a
30-day
with
either
normal
or
rapamycin-treated
diet.
After
chelation,
some
F0
females
crossed
males
produce
F1
offspring.
Physiological,
biochemical,
gene
expression
changes
assessed
in
after
days
chelation
30
interventions.
Post-eclosion
evaluations
conducted
flies,
along
60-day
survival
generations.
Result:
In
females,
significantly
reduced
(p
<
0.0001)
body
weight,
levels,
enzyme
while
increasing
GSH
levels.
Gene
showed
significant
0.05)
storage
(
Fer1HCH),
autophagy
(
ATG1),
telomere-related
genes
(
dHeT-A,
dTahre,
dTart).
A
partially
restored
levels
survival,
improved
antioxidants
but
had
mixed
expression.
male/female
exhibited
reduced/increased
respectively,
also
increased
median
weight
female
their
survival.
Conclusion:
has
lasting
effects,
diets
restoring
enhances
defenses
reduces
particularly
females.
Language: Английский
Professional phagocytes are recruited for the clearance of obsolete nonprofessional phagocytes in the Drosophila ovary
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: June 27, 2024
Cell
death
is
an
important
process
in
the
body,
as
it
occurs
throughout
every
tissue
during
development,
disease,
and
regeneration.
Phagocytes
are
responsible
for
clearing
away
dying
cells
typically
characterized
either
professional
or
nonprofessional
phagocytes.
Professional
phagocytes,
such
macrophages,
found
nearly
part
of
body
while
epithelial
cells,
type.
However,
there
organs
that
considered
“immune-privileged”
they
have
little
to
no
immune
surveillance
rely
on
phagocytes
engulf
cells.
These
surrounded
by
barriers
protect
from
viruses,
bacteria,
perhaps
even
The
Drosophila
ovary
immune-privileged,
however
presence
hemocytes,
macrophages
,
around
suggests
may
a
potential
function.
Here
we
analyze
hemocyte
localization
functions
response
starvation-induced
cell
ovary.
Hemocytes
were
accumulate
oviduct
vicinity
mature
eggs
follicle
debris.
Genetic
ablation
hemocytes
revealed
affects
oogenesis
phagocytose
ovarian
debris
their
absence
fecundity
decreases.
Unpaired3,
IL-6
like
cytokine,
was
be
required
recruitment
clear
obsolete
findings
demonstrate
role
ovary,
providing
more
thorough
understanding
phagocyte
communication
clearance
previously
thought
immune-privileged
organ.
Language: Английский
Glia-mediated gut-brain cytokine signaling couples sleep to intestinal inflammation
Alina Malita,
No information about this author
Olga I. Kubrak,
No information about this author
Xiaokang Chen
No information about this author
et al.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 30, 2024
Abstract
Sickness-induced
sleep
is
a
behavior
conserved
across
species
that
promotes
recovery
from
illness,
yet
the
underlying
mechanisms
are
poorly
understood.
Here,
we
show
interleukin-6-like
cytokine
signaling
Drosophila
gut
to
brain
glial
cells
regulates
sleep.
Under
healthy
conditions,
this
pathway
wakefulness.
However,
elevated
in
response
oxidative
stress
–
triggered
by
immune
and
inflammatory
responses
intestine
induces
The
cytokines
Unpaired
2
-3
upregulated
enteroendocrine
activate
JAK-STAT
cells,
including
those
of
blood-brain
barrier
(BBB).
This
activity
maintains
during
oxidative-stress-induced
intestinal
disturbances,
suggesting
glia
inhibits
wake-promoting
facilitate
sleep-dependent
restoration
under
these
conditions.
We
find
enteric
peptide
Allatostatin
A
(AstA)
enhances
wakefulness,
stress,
gut-derived
2/3
AstA
receptor
expression
BBB
glia,
thereby
sustaining
an
state
inflammation
or
illness.
Taken
together,
our
work
identifies
gut-to-glial
communication
couples
with
homeostasis
disease,
enhancing
sickness,
contributes
understanding
how
disturbances
arise
gastrointestinal
disturbances.
Language: Английский
Hormonal regulation and disruption in invertebrates – an historical perspective and recent findings
Molecular and Cellular Endocrinology,
Journal Year:
2024,
Volume and Issue:
593, P. 112335 - 112335
Published: July 30, 2024
Language: Английский
Glia-mediated gut-brain cytokine signaling couples sleep to intestinal inflammation
Alina Malita,
No information about this author
Olga I. Kubrak,
No information about this author
Xiaokang Chen
No information about this author
et al.
Published: Sept. 18, 2024
Sickness-induced
sleep
is
a
behavior
conserved
across
species
that
promotes
recovery
from
illness,
yet
the
underlying
mechanisms
are
poorly
understood.
Here,
we
show
interleukin-6-like
cytokine
signaling
Drosophila
gut
to
brain
glial
cells
regulates
sleep.
Under
healthy
conditions,
this
pathway
wakefulness.
However,
elevated
in
response
oxidative
stress
–
triggered
by
immune
and
inflammatory
responses
intestine
induces
The
cytokines
Unpaired
2
-3
upregulated
enteroendocrine
activate
JAK-STAT
cells,
including
those
of
blood-brain
barrier
(BBB).
This
activity
maintains
during
oxidative-stress-induced
intestinal
disturbances,
suggesting
glia
inhibits
wake-promoting
facilitate
sleep-dependent
restoration
under
these
conditions.
We
find
enteric
peptide
Allatostatin
A
(AstA)
enhances
wakefulness,
stress,
gut-derived
2/3
AstA
receptor
expression
BBB
glia,
thereby
sustaining
an
state
inflammation
or
illness.
Taken
together,
our
work
identifies
gut-to-glial
communication
couples
with
homeostasis
disease,
enhancing
sickness,
contributes
understanding
how
disturbances
arise
gastrointestinal
disturbances.
Language: Английский
Glia-mediated gut-brain cytokine signaling couples sleep to intestinal inflammation
Alina Malita,
No information about this author
Olga I. Kubrak,
No information about this author
Xiaokang Chen
No information about this author
et al.
Published: Sept. 18, 2024
Sickness-induced
sleep
is
a
behavior
conserved
across
species
that
promotes
recovery
from
illness,
yet
the
underlying
mechanisms
are
poorly
understood.
Here,
we
show
interleukin-6-like
cytokine
signaling
Drosophila
gut
to
brain
glial
cells
regulates
sleep.
Under
healthy
conditions,
this
pathway
wakefulness.
However,
elevated
in
response
oxidative
stress
–
triggered
by
immune
and
inflammatory
responses
intestine
induces
The
cytokines
Unpaired
2
-3
upregulated
enteroendocrine
activate
JAK-STAT
cells,
including
those
of
blood-brain
barrier
(BBB).
This
activity
maintains
during
oxidative-stress-induced
intestinal
disturbances,
suggesting
glia
inhibits
wake-promoting
facilitate
sleep-dependent
restoration
under
these
conditions.
We
find
enteric
peptide
Allatostatin
A
(AstA)
enhances
wakefulness,
stress,
gut-derived
2/3
AstA
receptor
expression
BBB
glia,
thereby
sustaining
an
state
inflammation
or
illness.
Taken
together,
our
work
identifies
gut-to-glial
communication
couples
with
homeostasis
disease,
enhancing
sickness,
contributes
understanding
how
disturbances
arise
gastrointestinal
disturbances.
Language: Английский