Muscle Wasting and Impaired Muscle Regeneration in a Murine Model of Chronic Pulmonary Inflammation

Langen, Ramon; Schols, A.M.W.J.; Kelders, Marco; Velden, Jos van der; Wouters, Emiel F.M.; Janssen–Heininger, Yvonne M. W.

doi:10.1165/rcmb.2006-0103oc

Cited by 107 publications

(116 citation statements)

References 43 publications

(59 reference statements)

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“…These and other systemic abnormalities can be reproduced with both smoke exposure and elastase challenge protocols (Gosker et al 2009, Lüthje et al 2009). Cigarette smoke induces weight loss, muscle atrophy, changes in muscle fiber type, and systemic inflammation, as well as reduces strength and endurance in experimental animals (Langen et al 2006, De Paepe et al 2008, Gosker et al 2009, similarly to what occurs in humans. Few data are available regarding these aspects in elastase models (Lewis et al 1992, Marchand et al 2000, Degens et al 2007, Lüthje et al 2009).…”

Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 97%

“…Pulmonary cachexia is associated with lung inflammation (Keatings et al 1996) and increased levels of circulating inflammatory cytokines (Di Francia et al 1994, Takabatake et al 2000, Eid et al 2001, suggesting that systemic inflammation could trigger or contribute to muscle atrophy (Langen et al 2006). These and other systemic abnormalities can be reproduced with both smoke exposure and elastase challenge protocols (Gosker et al 2009, Lüthje et al 2009).…”

Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 99%

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Elastase-induced pulmonary emphysema: insights from experimental models

Antunes

Rocco

2011

An. Acad. Bras. Ciênc.

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Several distinct stimuli can be used to reproduce histological and functional features of human emphysema, a leading cause of disability and death. Since cigarette smoke is the main cause of emphysema in humans, experimental researches have attempted to reproduce this situation. However, this is an expensive and cumbersome method of emphysema induction, and simpler, more efficacious alternatives have been sought. Among these approaches, elastolytic enzymes have been widely used to reproduce some characteristics of human cigarette smoke-induced disease, such as: augmentation of airspaces, inflammatory cell influx into the lungs, and systemic inflammation. Nevertheless, the use of elastase-induced emphysema models is still controversial, since the disease pathways involved in elastase induction may differ from those occurring in smoke-induced emphysema. This indicates that the choice of an emphysema model may impact the results of new therapies or drugs being tested. The aim of this review is to compare the mechanisms of disease induction in smoke and elastase emphysema models, to describe the differences among various elastase models, and to establish the advantages and disadvantages of elastase-induced emphysema models. More studies are required to shed light on the mechanisms of elastase-induced emphysema.

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Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 97%

Section: Elastase Vs Smoke-induced Emphysemamentioning

confidence: 99%

Elastase-induced pulmonary emphysema: insights from experimental models

Antunes

Rocco

2011

An. Acad. Bras. Ciênc.

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“…This is particularly true with TNFα, which promotes muscle wasting by enhancing the activity of the ubiquitin proteasome pathway (Langen et al 2006). TNFα also promotes muscle wasting by inducing apoptosis (Carbo et al 2002).…”

Section: Infl Ammationmentioning

confidence: 98%

Skeletal Muscle Dysfunction in Patients with Chronic Obstructive Pulmonary Disease

2010

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Chronic obstructive pulmonary disease (COPD) is a debilitating disease characterized by infl ammation-induced airfl ow limitation and parenchymal destruction. In addition to pulmonary manifestations, patients with COPD develop systemic problems, including skeletal muscle and other organ-specifi c dysfunctions, nutritional abnormalities, weight loss, and adverse psychological responses. Patients with COPD often complain of dyspnea on exertion, reduced exercise capacity, and develop a progressive decline in lung function with increasing age. These symptoms have been attributed to increases in the work of breathing and in impairments in gas exchange that result from airfl ow limitation and dynamic hyperinfl ation. However, there is mounting evidence to suggest that skeletal muscle dysfunction, independent of lung function, contributes signifi cantly to reduced exercise capacity and poor quality of life in these patients. Limb and ventilatory skeletal muscle dysfunction in COPD patients has been attributed to a myriad of factors, including the presence of low grade systemic infl ammatory processes, nutritional depletion, corticosteroid medications, chronic inactivity, age, hypoxemia, smoking, oxidative and nitrosative stresses, protein degradation and changes in vascular density. This review briefl y summarizes the contribution of these factors to overall skeletal muscle dysfunction in patients with COPD, with particular attention paid to the latest advances in the fi eld. Keywords: skeletal muscles, chronic obstructive pulmonary disease, diaphragm, quadriceps, fatigue, disuse, atrophy, smoking, exercise It has long been recognized that COPD is a systemic disease in which several extrapulmonary manifestations, including cachexia and skeletal muscle dysfunction, contribute to morbidity and mortality. Functionally, skeletal muscle dysfunction in COPD patients is characterized by signifi cant reduction in muscle strength and endurance. It is structurally characterized by loss of muscle mass and cross-sectional area (muscle atrophy), fi ber type distribution (reduction in the proportion of oxidative fi bers and increases in the proportion of glycolytic fi bers), oxidative metabolic capacity (attenuation of mitochondrial enzyme activities and expression) and capillary distribution (signifi cant loss of capillary density). Although disuse and inactivity are important contributors to the pathogenesis of skeletal muscle dysfunction in COPD patients, several other systemic and local factors are also involved. These include systemic infl ammation, malnutrition, corticosteroid usage, hypoxemia, aging, smoking and local factors such as the production of reactive oxygen (ROS) and nitrogen species (RNS) and enhanced protein degradation inside muscle fi bers, a result of increased activities of the proteasomal and lysosomal pathways and activation of calpains and caspases. Evidence of skeletal muscle dysfunction in patients with COPDIt has been well established that skeletal muscle function (strength and endurance) and s...

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“…In vivo data also support a role for TNF-␣ in inhibiting muscle differentiation following injury caused by modified muscle use. Expression of a lung-specific, TNF-␣ transgene that elevated systemic TNF-␣ attenuated the expression of dMyHC in mice subjected to hindlimb unloading followed by 3 to 5 days of muscle reloading (50). However, even these generally proproliferative, differentiation-suppressing effects of TNF-␣ are not always observed in muscle, and this variability may result from whether TNF-␣-induced effects are mediated through NF-B or other signaling pathways in muscle.…”

Section: Do Neutrophil-derived or M1 Macrophage-derived Molecules Modmentioning

confidence: 99%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

870

962

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Tidball JG, Villalta SA. Regulatory interactions between muscle and the immune system during muscle regeneration. Am J Physiol Regul Integr Comp Physiol 298: R1173-R1187, 2010. First published March 10, 2010 doi:10.1152/ajpregu.00735.2009.-Recent discoveries reveal complex interactions between skeletal muscle and the immune system that regulate muscle regeneration. In this review, we evaluate evidence that indicates that the response of myeloid cells to muscle injury promotes muscle regeneration and growth. Acute perturbations of muscle activate a sequence of interactions between muscle and inflammatory cells. The initial inflammatory response is a characteristic Th1 inflammatory response, first dominated by neutrophils and subsequently by CD68 ϩ M1 macrophages. M1 macrophages can propagate the Th1 response by releasing proinflammatory cytokines and cause further tissue damage through the release of nitric oxide. Myeloid cells in the early Th1 response stimulate the proliferative phase of myogenesis through mechanisms mediated by TNF-␣ and IL-6; experimental prolongation of their presence is associated with delayed transition to the early differentiation stage of myogenesis. Subsequent invasion by CD163ϩ /CD206 ϩ M2 macrophages attenuates M1 populations through the release of anti-inflammatory cytokines, including IL-10. M2 macrophages play a major role in promoting growth and regeneration; their absence greatly slows muscle growth following injury or modified use and inhibits muscle differentiation and regeneration. Chronic muscle injury leads to profiles of macrophage invasion and function that differ from acute injuries. For example, mdx muscular dystrophy yields invasion of muscle by M1 macrophages, but their early invasion is accompanied by a subpopulation of M2a macrophages. M2a macrophages are IL-4 receptor ϩ /CD206 ϩ cells that reduce cytotoxicity of M1 macrophages. Subsequent invasion of dystrophic muscle by M2c macrophages is associated with progression of the regenerative phase in pathophysiology. Together, these findings show that transitions in macrophage phenotype are an essential component of muscle regeneration in vivo following acute or chronic muscle damage. skeletal muscle; macrophage; neutrophil; muscular dystrophy; chemokines SKELETAL MUSCLE HAS A REMARKABLE capacity for repair, even following severe damage. Experimental findings show that crushing muscle, killing muscle by the injection of toxins, mechanical destruction caused by large, lengthening stretches, or killing muscle fibers by freezing can be followed by the successful regeneration of muscle that leads to recovery of normal structure and function. The regenerative capacity of skeletal muscle relies largely on the presence of a population of mononucleated, myogenic cells, called satellite cells, that retain their ability to proliferate and then differentiate to either fuse with existing fibers or with other myogenic cells to generate new fibers. Thus, perturbations to the processes that normally regulate the activation, proliferat...

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Muscle Wasting and Impaired Muscle Regeneration in a Murine Model of Chronic Pulmonary Inflammation

Cited by 107 publications

References 43 publications

Elastase-induced pulmonary emphysema: insights from experimental models

Elastase-induced pulmonary emphysema: insights from experimental models

Skeletal Muscle Dysfunction in Patients with Chronic Obstructive Pulmonary Disease

Regulatory interactions between muscle and the immune system during muscle regeneration

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