Role of Immune Cells in Animal Models for Inherited Peripheral Neuropathies

2006 ◽  
Vol 8 (1-2) ◽  
pp. 175-190 ◽  
Author(s):  
Chi Wang Ip ◽  
Antje Kroner ◽  
Stefan Fischer ◽  
Martin Berghoff ◽  
Igor Kobsar ◽  
...  
2006 ◽  
Vol 8 (1-2) ◽  
pp. 175-189 ◽  
Author(s):  
Chi Wang Ip ◽  
Antje Kroner ◽  
Stefan Fischer ◽  
Martin Berghoff ◽  
Igor Kobsar ◽  
...  

2020 ◽  
Vol 20 (4) ◽  
pp. 272-276
Author(s):  
Rachel Coomey ◽  
Rianne Stowell ◽  
Ania Majewska ◽  
Daniela Tropea

The development of new therapeutics is critically dependent on an understanding of the molecular pathways, the disruption of which results in neurological symptoms. Genetic and biomarker studies have highlighted immune signalling as a pathway that is impaired in patients with neurodevelopmental disorders (NDDs), and several studies on animal models of aberrant neurodevelopment have implicated microglia, the brain’s immune cells, in the pathology of these diseases. Despite the increasing awareness of the role of immune responses and inflammation in the pathophysiology of NDDs, the testing of new drugs rarely considers their effects in microglia. In this brief review, we present evidence of how the study of microglia can be critical for understanding the mechanisms of action of candidate drugs for NDDs and for increasing their therapeutic effect.


2002 ◽  
Vol 200 (4) ◽  
pp. 405-414 ◽  
Author(s):  
Mathias Maurer ◽  
Igor Kobsar ◽  
Martin Berghoff ◽  
Christoph D. Schmid ◽  
Stefano Carenini ◽  
...  

2013 ◽  
Vol 394 (12) ◽  
pp. 1571-1581 ◽  
Author(s):  
Benoit Barrette ◽  
Klaus-Armin Nave ◽  
Julia M. Edgar

Abstract Myelinating cells wrap axons with multi-layered myelin sheaths for rapid impulse propagation. Dysfunctions of oligodendrocytes or Schwann cells are often associated with neuroinflammation, as observed in animal models of leukodystrophies and peripheral neuropathies, respectively. The neuroinflammatory response modulates the pathological changes, including demyelination and axonal injury, but also remyelination and repair. Here we discuss different immune mechanisms as well as factors released or exposed by myelinating glia in disease conditions. The spectrum of inflammatory mediators varies with different myelin disorders and has a major impact on the beneficial or detrimental role of immune cells in keeping nervous system integrity.


2020 ◽  
Vol 48 (3) ◽  
pp. 167-178
Author(s):  
Jessica SY Lim ◽  
Peter CA Kam

This narrative review aims to describe the role of peripheral and central immune responses to tissue and nerve damage in animal models, and to discuss the use of immunomodulatory agents in clinical practice and their perioperative implications. Animal models of pain have demonstrated that nerve injury activates immune signalling pathways that drive aberrant sensory processes, resulting in neuropathic and chronic pain. This response involves the innate immune system. T lymphocytes are also recruited. Glial cells surrounding the damaged nerves release cytokines and proinflammatory mediators that activate resident immune cells and recruit circulatory immune cells. Toll-like receptors on the glial cells play a crucial role in the pathogenesis of chronic pain. Animal models indicate an immune mechanism of neuropathic pain. Analgesic drugs and anaesthetic agents have varied effects on the neuroimmune interface. Evidence of a neuroimmune interaction is mainly from animal studies. Human studies are required to evaluate the clinical implications of this neuroimmune interaction.


2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Reka Kugyelka ◽  
Zoltan Kohl ◽  
Katalin Olasz ◽  
Katalin Mikecz ◽  
Tibor A. Rauch ◽  
...  

Rheumatoid arthritis (RA) is one of the most common autoimmune disorders characterized by the chronic and progressive inflammation of various organs, most notably the synovia of joints leading to joint destruction, a shorter life expectancy, and reduced quality of life. Although we have substantial information about the pathophysiology of the disease with various groups of immune cells and soluble mediators identified to participate in the pathogenesis, several aspects of the altered immune functions and regulation in RA remain controversial. Animal models are especially useful in such scenarios. Recently research focused on IL-17 and IL-17 producing cells in various inflammatory diseases such as in RA and in different rodent models of RA. These studies provided occasionally contradictory results with IL-17 being more prominent in some of the models than in others; the findings of such experimental setups were sometimes inconclusive compared to the human data. The aim of this review is to summarize briefly the recent advancements on the role of IL-17, particularly in the different rodent models of RA.


Author(s):  
Katelyn Donaldson ◽  
Ahmet Höke

There are numerous types of peripheral neuropathies and conditions that cause neuropathic pain with varying symptoms and different mechanisms of pathogenesis. Therefore, it is not surprising that many different animal models of peripheral neuropathies and neuropathic pain have been developed with varying degrees of fidelity to recapitulate the human disease. Nevertheless, these models are useful in a deconstructive manner to examine role of specific molecular pathways in pathogenesis of different types of peripheral neuropathies and test potential new drugs.


Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 717
Author(s):  
Abhishek Kulkarni ◽  
Jerry L. Nadler ◽  
Raghavendra G. Mirmira ◽  
Isabel Casimiro

Lipoxygenases (LOXs) are lipid metabolizing enzymes that catalyze the di-oxygenation of polyunsaturated fatty acids to generate active eicosanoid products. 12-lipoxygenases (12-LOXs) primarily oxygenate the 12th carbon of its substrates. Many studies have demonstrated that 12-LOXs and their eicosanoid metabolite 12-hydroxyeicosatetraenoate (12-HETE), have significant pathological implications in inflammatory diseases. Increased level of 12-LOX activity promotes stress (both oxidative and endoplasmic reticulum)-mediated inflammation, leading to damage in these tissues. 12-LOXs are also associated with enhanced cellular migration of immune cells—a characteristic of several metabolic and autoimmune disorders. Genetic depletion or pharmacological inhibition of the enzyme in animal models of various diseases has shown to be protective against disease development and/or progression in animal models in the setting of diabetes, pulmonary, cardiovascular, and metabolic disease, suggesting a translational potential of targeting the enzyme for the treatment of several disorders. In this article, we review the role of 12-LOXs in the pathogenesis of several diseases in which chronic inflammation plays an underlying role.


2016 ◽  
Author(s):  
M Mannelli ◽  
E Rapizzi ◽  
L Canu ◽  
T Ercolino ◽  
V Giache
Keyword(s):  

2019 ◽  
Vol 24 (45) ◽  
pp. 5367-5374 ◽  
Author(s):  
Xiaoyun Li ◽  
Seyed M. Moosavi-Basri ◽  
Rahul Sheth ◽  
Xiaoying Wang ◽  
Yu S. Zhang

The role of endovascular interventions has progressed rapidly over the past several decades. While animal models have long-served as the mainstay for the advancement of this field, the use of in vitro models has become increasingly widely adopted with recent advances in engineering technologies. Here, we review the strategies, mainly including bioprinting and microfabrication, which allow for fabrication of biomimetic vascular models that will potentially serve to supplement the conventional animal models for convenient investigations of endovascular interventions. Besides normal blood vessels, those in diseased states, such as thrombosis, may also be modeled by integrating cues that simulate the microenvironment of vascular disorders. These novel engineering strategies for the development of biomimetic in vitro vascular structures will possibly enable unconventional means of studying complex endovascular intervention problems that are otherwise hard to address using existing models.


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