Complement Activation Promotes Muscle Inflammation during Modified Muscle Use

Frenette, Jérôme; Cai, Baiyuan; Tidball, James G.

doi:10.1016/s0002-9440(10)65081-x

Cited by 86 publications

(91 citation statements)

References 35 publications

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“…For example, in the early phase following EC, focal degenerative and inflammatory responses in damaged muscle fiber are accompanied by alteration of membrane depolarization [35] and fiber edema [16]. Previous studies [26,36] also demonstrated the presence of necrotic muscle fibers with macrophage invasion at 1 to 3 days after injury and muscle fiber regeneration with myoblasts and myotubes at 4 days after [37]. These physiological and structural changes may contribute to the determination of EMG parameters.…”

Section: Consideration Of An Experimental Modelmentioning

confidence: 94%

Histological Skeletal Muscle Damage and Surface EMG Relationships Following Eccentric Contractions

et al. 2008

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This study examined the effects of a different number of eccentric contractions (ECs) on histological characteristics, surface electromyogram (EMG) parameters (integral EMG, iEMG; muscle fiber conduction velocity, MFCV; and action potential waveform), and isometric peak torque using the rat EC model. Male Wistar rats (n = 40) were anesthetized, and ECs were initiated in the tibialis anterior muscle via electrical stimulation while the muscle was being stretched by electromotor. The rats were grouped according to the number of ECs (EC1, EC5, EC10, EC20, EC30, EC40, and EC100). Three days after the ECs, surface EMG signals and isometric peak torque were measured during evoked twitch contractions via electrical stimulation of the peroneal nerve. The muscle damage was evaluated from hematoxylin-eosin (HE) stained cross sections as a relative number of damaged fibers to intact fibers. Intense histological muscle damage (approximately 50% to 70% of the fiber), loss of isometric peak torque, disturbance of action potential waveform, and depression of iEMG (approximately -60% to -70%) were observed at EC20, EC30, EC40, and EC100. On the other hand, the MFCV did not change in any EC group. Although muscle damage and pathological surface EMG signals were not found at EC10, isometric peak torque was reduced significantly. In conclusion, the extent of histological muscle damage is not proportionally related to the number of ECs. Muscle damage was reflected by iEMG and action potential waveforms, but not by MFCV, which remained unaffected even though approximately 50% to 70% of the fiber demonstrated injury.

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Section: Consideration Of An Experimental Modelmentioning

confidence: 94%

Histological Skeletal Muscle Damage and Surface EMG Relationships Following Eccentric Contractions

et al. 2008

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“…Injections are expected to produce an inflammatory response, as expressed by increased CD43þ cells by 6 h and ED1þ and ED2þ cells by 24 h. 40,41 Eighty-four rats in seven treatment or control groups were injected or observed (no-injection control group) at baseline and assessed at 6, 24, and 72 h postinjection using immunohistochemistry (IHC) and quantitative polymerase chain reaction (qPCR) analysis (Fig. 1).…”

Section: Methodsmentioning

confidence: 99%

“…CD43 has been previously used to identify neutrophils in rat muscle tissue. 41 However, it is not specific to neutrophils and has also been used previously as a T lymphocyte label.…”

Section: Ihcmentioning

confidence: 99%

Early inflammatory response of knee ligaments to prolotherapy in a rat model

Jensen

Rabago

Best

et al. 2008

Journal Orthopaedic Research

114

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Prolotherapy is an alternative injection-based therapy for chronic musculoskeletal pain. Three different proliferants, D-glucose (dextrose), phenol-glucose-glycerine (P2G), and sodium morrhuate, used in prolotherapy are hypothesized to strengthen and reorganize chronically injured soft tissue and decrease pain through modulation of the inflammatory process. Our hypothesis is that commonly used prolotherapy solutions will induce inflammation (leukocyte and macrophage infiltration) in medial collateral ligaments (MCLs) compared to needlestick, saline injection, and no-injection controls. MCLs of 84 Sprague-Dawley rats were injected one time at both the tibial and femoral insertions. Immunohistochemistry (IHC) was used to determine the inflammatory response at three locations (tibial and femoral insertions and midsubstance) 6, 24, and 72 h after dextrose injection compared to saline-and no-injection controls and collagenase (positive control) (n ¼ 4). qPCR was used to analyze gene expression 24 h postinjection (n ¼ 4). Sodium morrhuate, P2G, and needlestick control were also investigated after 24 h (n ¼ 4). In general, inflammation (CD43þ, ED1þ, and ED2þ cells) increased after prolotherapy injection compared to no-injection control but did not increase consistently compared to saline and needlestick control injections. This response varied by both location and proliferant. Inflammation was observed at 6 and 24 h postinjection but was resolved by 72 h compared to no-injection controls (p < 0.05). CD43þ leukocytes and ED2þ macrophages increased compared to needlestick and saline-injection control, respectively, 24 h postinjection (p < 0.05). Prolotherapy injections created an inflammatory response, but this response was variable and overall, not uniformly different from that caused by saline injections or needlestick procedures. ß

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“…As in other tissues, Ly6Cϩ/F4/80-neutrophils are the first responders and begin to appear at elevated numbers within 2 h of muscle damage, typically peaking in concentration between 6 and 24 h postinjury and then rapidly declining in numbers. Following the onset of neutrophil invasion, phagocytic macrophages begin to invade, reaching significantly elevated concentrations at about 24 h postinjury and continue to increase in numbers until about 2 days postinjury, when their numbers begin to decline sharply (8,16,26,80,98,109,117). Their invasion precedes the elevation of a population of nonphagocytic macrophages that reaches peak concentrations in the muscle at about 4 days postinjury but remains significantly elevated for many days (Fig.…”

Section: Changes In Myeloid Cell Phenotype In Muscle Following Injurymentioning

confidence: 97%

“…Desmin, a muscle-specific intermediate protein, is a candidate signaling molecule because it is rapidly lost from muscle fibers following injury (55), and it is able to activate the complement system (57), which provides an extremely rapid mechanism for initiating the innate immune response. Furthermore, blocking complement activation by systemic administration of soluble complement receptor-1 prior to muscle injury reduces muscle inflammation and damage (26).…”

Section: What Initiates the Th1 Inflammatory Response In Injured Muscle?mentioning

confidence: 99%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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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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Complement Activation Promotes Muscle Inflammation during Modified Muscle Use

Cited by 86 publications

References 35 publications

Histological Skeletal Muscle Damage and Surface EMG Relationships Following Eccentric Contractions

Histological Skeletal Muscle Damage and Surface EMG Relationships Following Eccentric Contractions

Early inflammatory response of knee ligaments to prolotherapy in a rat model

Regulatory interactions between muscle and the immune system during muscle regeneration

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