Interactions between neutrophils and macrophages promote macrophage killing of rat muscle cells in vitro

Nguyen, Hal X.; Tidball, James G.

doi:10.1113/jphysiol.2002.031450

Cited by 124 publications

(99 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…NO has been implicated in acute muscle damage in various experimental models in vivo and in cell culture. Muscle cells cocultured with both neutrophils and macrophages developed a NO-dependent cytotoxic process [32], and inhibition of NOS by L-NAME decreased the extent of muscle cell damage in an experimental model of modifi ed muscle use [33], as well as in models of muscle crush injury [34]. Furthermore, knockout mice for iNOS develop less muscle injury in a model of ischemia-reperfusion [35].…”

Section: Discussionmentioning

confidence: 99%

Role of nitric oxide in the local and systemic pathophysiological effects induced by Bothrops asper snake venom in mice

2006

View full text Add to dashboard Cite

Abstract.Objective: To assess the role of nitric oxide in the most relevant local and systemic manifestations in mice injected with the venom of the snake Bothrops asper. Mice were pretreated with nitric oxide synthase inhibitors, and the modifi cations of the pathological effects induced by the venom were tested. Results: Inhibition of NO synthesis did not affect acute local myonecrosis and hemorrhage in muscle tissue upon intramuscular injection of venom. Local footpad edema was reduced in mice pretreated with the NO synthase inhibitor L-NAME, and a reduction in the extent of infl ammatory infi ltrate in muscle tissue was observed after envenomation in mice pretreated with L-NAME and aminoguanidine. The most pronounced effect of NOS inhibition by L-NAME was an increment in the lethal activity of the venom, when injected by the intraperitoneal route. Conclusion: Nitric oxide does not seem to play a signifi cant role in the local acute pathological alterations (hemorrhage and myonecrosis) induced by B. asper venom in mice, although it contributes to edema and infl ammatory infi ltrate. Nitric oxide exerts a protective role in the systemic pathophysiological manifestations leading to lethality.

show abstract

Section: Discussionmentioning

confidence: 99%

Role of nitric oxide in the local and systemic pathophysiological effects induced by Bothrops asper snake venom in mice

2006

View full text Add to dashboard Cite

show abstract

“…31 for review). M1 macrophages can also promote muscle damage in vitro and in vivo by the production of cytotoxic levels of nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) (77,123). Early studies of muscle inflammation using the rodent hindlimb suspension/reloading model (HS/Rel) implicated M1 macrophages in the early stages of muscle injury (63,64,109).…”

Section: Phenotypic Diversity Of Macrophages In Regenerative Skeletalmentioning

confidence: 99%

“…This may be one of several important regulatory interactions that occur between neutrophils and M1 macrophages during the early stage of muscle inflammation. For example, neutrophils can also promote the cytolytic capacity of macrophages to lyse muscle cells (77). This elevated lysis of muscle cells can then provide positive feedback to further promote phagocytic activity of macrophages that is stimulated by myoblast lysis (97).…”

Section: M1 Macrophages Express Cd68mentioning

confidence: 99%

Regulatory interactions between muscle and the immune system during muscle regeneration

Tidball

Villalta

2010

American Journal of Physiology-Regulatory, Integrative and Comp

905

987

View full text Add to dashboard Cite

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...

show abstract

“…Neutrophils are also prominent constituents of the inflammatory infiltrate of injured muscle, invading within hours of injury (Fielding et al, 1993). Neutrophils produce high levels of free radicals that can lyse muscle membranes and exacerbate damage caused by M1 macrophages (Nguyen and Tidball, 2003). Neutrophils may also contribute to muscle regeneration by phagocytosis of tissue debris and by releasing cytokines that regulate the inflammatory response.…”

Section: The Role Of Other Myeloid Cells In Regenerationmentioning

confidence: 99%

Shared signaling systems in myeloid cell-mediated muscle regeneration

2014

View full text Add to dashboard Cite

Much of the focus in muscle regeneration has been placed on the identification and delivery of stem cells to promote regenerative capacity. As those efforts have advanced, we have learned that complex features of the microenvironment in which regeneration occurs can determine success or failure. The immune system is an important contributor to that complexity and can determine the extent to which muscle regeneration succeeds. Immune cells of the myeloid lineage play major regulatory roles in tissue regeneration through two general, inductive mechanisms: instructive mechanisms that act directly on muscle cells; and permissive mechanisms that act indirectly to influence regeneration by modulating angiogenesis and fibrosis. In this article, recent discoveries that identify inductive actions of specific populations of myeloid cells on muscle regeneration are presented, with an emphasis on how processes in muscle and myeloid cells are co-regulated. KEY WORDS: Muscle regeneration, Macrophage phenotype, Signaling systems IntroductionAcute trauma, chronic disease or disruption of vascularization cause rapid death of skeletal muscle. Functional recovery of the damaged tissue is determined by interacting cellular responses, including stem cell activation, proliferation and differentiation, vascular repair, and tissue fibrosis during healing. Experimental approaches to improve muscle regeneration have focused on identifying stem cell populations that promote regeneration and refining their delivery, while using genetic or pharmacological manipulations to influence angiogenesis and fibrosis. However, those approaches are sensitive to the presence of myeloid cells in the injured muscle, suggesting that manipulations of myeloid cells can provide novel strategies to potentiate muscle regeneration. As knowledge of myeloid cell involvement in muscle regeneration has grown, we have come to appreciate that multiple subpopulations interact in complex and delicately balanced ways to influence regeneration. Perturbations in myeloid cell number, phenotype or the stage of regeneration at which they are present can yield vastly different outcomes in the regenerative process. As these complexities become better understood, there is hope that knowledge can be exploited to improve muscle regeneration therapy.In this Review, inductive processes through which myeloid cells influence muscle regeneration are presented, including instructive processes that directly influence developmental gene expression in muscle and permissive processes that modify the environment in which regeneration occurs. Here, muscle 'regeneration' refers to processes in damaged muscle tissue that lead to the restoration of normal structure and homeostasis, especially those events that influence the differentiation and growth of muscle cells that replace damaged tissue (Box 1). In addition, we emphasize discoveries that have contributed to understanding the mechanisms that coordinate phenotypic switches in myeloid cell populations with progressive stages of musc...

show abstract

Interactions between neutrophils and macrophages promote macrophage killing of rat muscle cells in vitro

Cited by 124 publications

References 32 publications

Role of nitric oxide in the local and systemic pathophysiological effects induced by Bothrops asper snake venom in mice

Role of nitric oxide in the local and systemic pathophysiological effects induced by Bothrops asper snake venom in mice

Regulatory interactions between muscle and the immune system during muscle regeneration

Shared signaling systems in myeloid cell-mediated muscle regeneration

Contact Info

Product

Resources

About