Differential cytokine gene expression in the diaphragm in response to strenuous resistive breathing.

@article{Vassilakopoulos2004DifferentialCG,
  title={Differential cytokine gene expression in the diaphragm in response to strenuous resistive breathing.},
  author={Theodoros P. Vassilakopoulos and Maziar Divangahi and George Rallis and Osama A Kishta and Basil J Petrof and Alain Steve Comtois and Sabah N A Hussain},
  journal={American journal of respiratory and critical care medicine},
  year={2004},
  volume={170 2},
  pages={
          154-61
        }
}
Strenuous resistive breathing induces plasma cytokines that do not originate from circulating monocytes. We hypothesized that cytokine production is induced inside the diaphragm in response to resistive loading. Anesthetized, tracheostomized, spontaneously breathing Sprague-Dawley rats were subjected to 1, 3, or 6 hours of inspiratory resistive loading, corresponding to 45-50% of the maximum inspiratory pressure. Unloaded sham-operated rats breathing spontaneously served as control animals. The… 

Figures from this paper

Impact of IL-10 on diaphragmatic cytokine expression and contractility during Pseudomonas Infection.
TLDR
Shifting the balance between pro- and anti-inflammatory mediators in favor of the latter by IL-10 gene delivery was able to restore normal diaphragmatic force-generating capacity under these conditions, suggesting a possible avenue for therapeutic intervention.
Nitric oxide regulates cytokine induction in the diaphragm in response to inspiratory resistive breathing.
TLDR
It is hypothesized that endogenously produced NO downregulates IRB-induced cytokine production in the strenuously contracting diaphragm through its action on MAPKs and NF-κB.
Ventilatory muscle activation and inflammation: cytokines, reactive oxygen species, and nitric oxide.
TLDR
Enhanced generation of reactive oxygen species, oxidative stress augmentation, reduced NO production, and glycogen depletion are potential stimuli for the cytokine induction that is secondary to strenuous diaphragmatic contractions.
Endotoxin triggers nuclear factor-kappaB-dependent up-regulation of multiple proinflammatory genes in the diaphragm.
TLDR
Constitutive and LPS-induced proinflammatory gene expression are exaggerated in the diaphragm compared with limb muscles and are critically dependent on the NF-kappaB pathway.
MAPKs and NF-κB differentially regulate cytokine expression in the diaphragm in response to resistive breathing: the role of oxidative stress.
TLDR
IRB-induced cytokine upregulation in the diaphragm is under the regulatory control of MAPKs and NF-κB, and IL-6 is regulated differently from all other cytokines through a P38-dependent and NF -κB independent pathway.
Inflammatory Events and Oxidant Production in the Diaphragm, Gastrocnemius, and Blood of Rats Exposed to Chronic Intermittent Hypoxia: Therapeutic Strategies
TLDR
Proinflammatory cytokines are differentially expressed in respiratory and limb muscles and plasma of CIH‐exposed rats, while superoxide anion production increased in both muscle types and blood, and infliximab and NAC exerted different effects.
Heat stroke activates a stress-induced cytokine response in skeletal muscle.
TLDR
It is demonstrated that skeletal muscle responds to HS with a distinct "stress-induced immune response," characterized by an early upregulation of IL-6, IL-10, and TLR-4 and suppression ofIL-1β and TNF-α mRNA, a pattern discrete from classic innate immune cytokine responses.
The immune response to resistive breathing: Implications for respiratory failure
TLDR
Resistive breathing is an “immune challenge” for the body, initiating an inflammatory response consisting of elevation of plasma cytokines and recruitment and activation of lymphocyte subpopulations, leading to production of adrenocorticotropic cytokines.
Free Radical Biology in Skeletal Muscle Ventilatory muscle activation and inflammation : cytokines , reactive oxygen species , and nitric oxide
TLDR
Enhanced generation of reactive oxygen species, oxidative stress augmentation, reduced NO production, and glycogen depletion are potential stimuli for the cytokine induction that is secondary to strenuous diaphragmatic contractions, and cytokine upregulation within the workingdiaphragm may be adaptive and maladaptive.
...
...

References

SHOWING 1-10 OF 83 REFERENCES
Strenuous resistive breathing induces plasma cytokines: role of antioxidants and monocytes.
TLDR
It is concluded that oxidative stress is a major stimulus for the resistive breathing-induced cytokine production and that monocytes play no role in this process.
Surgical manipulation, but not moderate exercise, is associated with increased cytokine mRNA expression in the rat soleus muscle.
TLDR
In conclusion, gentle surgical manipulation is a strong stimulus for IL-6 and IL-1beta mRNA synthesis in skeletal muscle, whereas exercise or electrical muscle stimulation at moderate intensity does not independently affect cytokine mRNA levels in the contracting soleus.
Tissue expression and plasma concentrations of TNFalpha, IL-1beta, and IL-6 following treadmill exercise in mice.
TLDR
The source of the plasma IL-6 following exercise does not appear to be lung, liver, muscle, or brain tissue, and remains to be determined, which suggests that tissue level cytokine expression may not necessarily lead to increased plasma cytokine concentrations.
Antioxidants attenuate the plasma cytokine response to exercise in humans.
TLDR
It is concluded that in untrained humans oxidative stress is a major stimulus for exercise-induced cytokine production and that monocytes play no role in this process.
Tissue expression and plasma concentrations of TNFα, IL-1β, and IL-6 following treadmill exercise in mice
TLDR
The source of the plasma IL-6 following exercise does not appear to be lung, liver, muscle, or brain tissue, and remains to be determined, which suggests that tissue level cytokine expression may not necessarily lead to increased plasma cytokine concentrations.
Differential expression of TNF-alpha, IL-6, and IGF-1 by graded mechanical stress in normal rat myocardium.
TLDR
The current data provide the first demonstration that TNF-alpha, IL-6, and IGF-1 ligand-receptor systems are differentially expressed within the normal rat myocardium in response to graded mechanical stretch.
Tumor necrosis factor and endotoxin do not directly affect in vitro diaphragm function.
TLDR
It is concluded that the impairment of diaphragm function during sepsis is not mediated by a direct effect of TNF or endotoxin, and any aspect of contractile function tested, including force-frequency characteristics, fatiguability, and recovery from fatigue.
Chronic beta-adrenergic stimulation induces myocardial proinflammatory cytokine expression.
TLDR
Chronic beta-adrenergic stimulation induces myocardial, but not systemic, elaboration of TNF-alpha, IL-1beta, and IL-6, and all 3 cytokines were readily detected throughout the myocardium in animals treated with isoproterenol.
Load-Dependent and -Independent Regulation of Proinflammatory Cytokine and Cytokine Receptor Gene Expression in the Adult Mammalian Heart
TLDR
Sustained hemodynamic overloading provokes a transient increase in proinflammatory cytokine and cytokine receptor gene expression; however, the decrease in pro inflammatory cytokine gene expression occurred in the absence of changes in loading conditions, suggesting that the expression of proinflammatoryinflammatory cytokines in the heart is regulated, at least in part, by load-dependent and load-independent mechanisms.
Tumor necrosis factor alpha decreases in vivo diaphragm contractility in dogs.
TLDR
It is concluded that TNF alpha infusion was associated with significant declines in isotonic and quasi-isometric diaphragm contraction and that this could be explained, at least in part, by impaired neuromuscular transmission.
...
...