scholarly journals Intracerebral injection of proinflammatory cytokines or leukocyte chemotaxins induces minimal myelomonocytic cell recruitment to the parenchyma of the central nervous system.

1992 ◽  
Vol 176 (1) ◽  
pp. 255-259 ◽  
Author(s):  
P B Andersson ◽  
V H Perry ◽  
S Gordon
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Leukocyte Adhesion ◽  
Platelet Activating Factor ◽  
Intracerebral Injection ◽  
Necrosis Factor Alpha ◽  
Cell Recruitment ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
Necrosis Factor

Neither excitotoxic neurodegeneration nor lipopolysaccharide induces an acute myelomonocytic exudate in the murine central nervous system (CNS) parenchyma (Andersson, P.-B., V. H. Perry, and S. Gordon. 1991. Neuroscience, 42:201; Andersson, P.-B., V. H. Perry, and S. Gordon. 1992. Neuroscience 48:169). In this study formyl-methionyl-leucyl-phenylalanine, platelet-activating factor, interleukin 8 (IL-8), IL-1, or tumor necrosis factor alpha were injected into the hippocampus to assess whether these leukocyte chemotaxins and known mediators of recruitment could bypass this block. They induced morphologic activation of microglia and widespread leukocyte margination but little or no cell exudation into the CNS parenchyma. By contrast, there was acute myelomonocytic cell recruitment to the choroid plexus, meninges, and ventricular system, comparable to that in the skin after subcutaneous injection. The normal CNS parenchyma appears to be a tissue unique in its resistance to leukocyte diapedesis, which is shown here to be at a step beyond chemotactic cytokine secretion or induction of leukocyte adhesion to cerebral endothelium.

scholarly journals Tumor necrosis factor alpha induces adhesion molecule expression on human fetal astrocytes.

1992 ◽  
Vol 176 (6) ◽  
pp. 1631-1636 ◽  
Author(s):  
A A Hurwitz ◽  
W D Lyman ◽  
M P Guida ◽  
T M Calderon ◽  
J W Berman
Keyword(s):  
Central Nervous System ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Tumor Necrosis ◽  
Leukocyte Adhesion ◽  
Necrosis Factor Alpha ◽  
The Central Nervous System ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Leukocyte Adhesion Molecules

Leukocyte adhesion molecules on endothelial cells of the blood-brain barrier may participate in the entry of leukocytes into the central nervous system. Because astrocytes are also a component of the blood-brain barrier and have been associated with inflammation, we studied the ability of astrocytes to express leukocyte adhesion molecules using Northern blot and immunocytochemical techniques. Astrocytes treated with the proinflammatory cytokine tumor necrosis factor alpha (TNF) expressed messenger RNA for the adhesion molecules E-selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1, as well as their corresponding proteins. In addition, TNF-treated astrocytes expressed a monocyte adhesion protein identified by our laboratory, recognized by the monoclonal antibody IG9. These results indicate that under inflammatory conditions in the central nervous system, such as multiple sclerosis and acquired immune deficiency syndrome, astrocyte expression of adhesion molecules may facilitate the migration of leukocytes and contribute to the disease process.

scholarly journals Pathological findings in central nervous system demyelination associated with infliximab

2019 ◽  
Vol 26 (9) ◽  
pp. 1124-1129 ◽  
Author(s):  
Alicja Kalinowska-Lyszczarz ◽  
Mahboobeh Fereidan-Esfahani ◽  
Yong Guo ◽  
Claudia F Lucchinetti ◽  
W Oliver Tobin
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tnf Alpha ◽  
Infliximab Treatment ◽  
Necrosis Factor Alpha ◽  
Immune Mediated ◽  
Central Nervous System Demyelination ◽  
Factor Alpha ◽  
Cns Demyelination ◽  
Necrosis Factor

Background: Tumor necrosis factor alpha (TNF-alpha) inhibitors, such as infliximab, are commonly used to treat rheumatoid arthritis (RA) and other immune-mediated disorders. Objective: To determine whether infliximab-associated central nervous system (CNS) demyelination can be differentiated from multiple sclerosis (MS). Methods: We present a case of pathologically proven CNS demyelination in a patient treated with infliximab and describe clinical–radiographic–neuropathological findings. Putative mechanisms of TNF-alpha inhibitor-associated CNS demyelination are described. Results and conclusion: Infliximab treatment is associated with CNS inflammatory demyelinating activity, which is histopathologically indistinguishable from MS.

scholarly journals Central Nervous System Demyelination Related to Tumour Necrosis Factor Alpha Inhibitor

2022 ◽  
Vol 8 (1) ◽  
pp. 205521732110707
Author(s):  
Shin Yee Chey ◽  
Allan G. Kermode
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background An association between tumour necrosis factor alpha (TNF-α) inhibitors exposure and central nervous system (CNS) demyelinating disorders has been postulated but is poorly understood. Objectives Describe the clinical spectrum and progress of a cohort of patients who developed demyelinating disorder following exposure to TNF-α inhibitor. Methods Retrospective chart review of patients who presented to a single neurologist in Western Australia between May 2003 and July 2020. Results 7 patients (6 females and 1 male) were identified. Mean age was 49.1 years. Mean follow-up time was 2.9 years. Mean interval between commencement of TNF-α inhibitor and onset of demyelinating event was 3 years. The spectrum of demyelinating events included transverse myelitis ( N = 3), acute brainstem syndrome ( N = 1) and optic neuritis ( N = 1). 2 patients had an atypical presentation but had MRI findings which unequivocally showed demyelinating changes. 2 patients had a monophasic event while the other 5 patients were diagnosed to have multiple sclerosis. All symptomatic patients with multiple sclerosis were started on disease modifying therapy and remained relapse free during follow-up. Conclusion Exposure to TNF-α inhibitor appears to increase the risk of demyelinating event. Whether TNFα inhibition directly results in CNS demyelination or trigger demyelination in susceptible individuals requires further research.

scholarly journals Demyelinating central nervous system lesions, following the use of tumor necrosis factor alpha antagonist

2018 ◽  
Vol 5 (5) ◽  
pp. 19
Author(s):  
Emmanuel Bogdos ◽  
Sofia Markoula ◽  
Anastasia Zikou ◽  
Paraskevi Voulgari ◽  
Aleksandros Drosos ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Alpha Antagonist ◽  
Necrosis Factor
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