Inflammatory processes play a key role in pathophysiology of many neurologic diseases/trauma, but the effect of immune cells and factors on neurotransplantation strategies remains unclear. We hypothesized that cellular and humoral components of innate immunity alter fate and migration of human neural stem cells (hNSC). In these experiments, conditioned media collected from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and promoted cell migration in vitro. PMN were shown to generate C1q and C3a; exposure of hNSC to PMN-synthesized concentrations of these complement proteins promoted astrogliogenesis and cell migration. Furthermore, in vitro, Abs directed against C1q and C3a reversed the fate and migration effects observed. In a proof-of-concept in vivo experiment, blockade of C1q and C3a transiently altered hNSC migration and reversed astroglial fate after spinal cord injury. Collectively, these data suggest that modulation of the innate/humoral inflammatory microenvironment may impact the potential of cell-based therapies for recovery and repair following CNS pathology.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5523578 | PMC |
| http://dx.doi.org/10.4049/jimmunol.1600064 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
C3/C3aR Bridges Spinal Astrocyte-Microglia Crosstalk and Accelerates Neuroinflammation in Morphine-Tolerant Rats.
CNS Neurosci Ther
January 2025
Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Aims: Communication within glial cells acts as a pivotal intermediary factor in modulating neuroimmune pathology. Meanwhile, an increasing awareness has emerged regarding the detrimental role of glial cells and neuroinflammation in morphine tolerance (MT). This study investigated the influence of crosstalk between astrocyte and microglia on the evolution of morphine tolerance.
View Article and Find Full Text PDFAberrant Complement Activation Is Associated With Structural Brain Damage in Multiple Sclerosis.
Neurol Neuroimmunol Neuroinflamm
March 2025
Department of Neurology with Institute of Translational Neurology, University Hospital 4 Münster, Germany.
Article Synopsis
- Elevated levels of activated complement proteins in cerebrospinal fluid (CSF) are linked to increased severity of multiple sclerosis (MS) and correlate with brain imaging and disease biomarkers.
- A study involving 239 patients analyzed various complement components and liquid biomarkers in CSF, finding specific proteins like C4a, Ba, and C3a strongly associated with accelerated brain atrophy and lesion formation.
- Results indicate that higher levels of these complement proteins are predictive of greater brain volume loss and increased development of lesions, suggesting their potential role as biomarkers for disease progression in MS.
The relationship between serum CTRP-5, C3a/desArg, and complement-C3 levels and hypothyroidism in women with polycystic ovary syndrome.
BMC Endocr Disord
December 2024
Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, P.O. Box: 1449614525, Tehran, Iran.
Article Synopsis
- This study explores the relationship between thyroid disorders and polycystic ovary syndrome (PCOS), highlighting similarities in energy metabolism and hormonal factors.
- It involved a case-control design with three groups: healthy women, women with PCOS and hypothyroidism, and women with PCOS without hypothyroidism, measuring various serum levels to assess thyroid function and related metabolic factors.
- Results showed that low levels of CTRP-5 and high levels of ASP and complement C3 in PCOS patients may indicate thyroid dysfunction, impacting lipid and glucose metabolism, suggesting a need for more research on hypothyroidism prevalence in PCOS.
Microglia mediate memory dysfunction via excitatory synaptic elimination in a fracture surgery mouse model.
J Neuroinflammation
September 2024
Department of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Cognitive impairment is a common issue among human patients undergoing surgery, yet the neural mechanism causing this impairment remains unidentified. Surgical procedures often lead to glial cell activation and neuronal hypoexcitability, both of which are known to contribute to postoperative cognitive dysfunction (POCD). However, the role of neuron-glia crosstalk in the pathology of POCD is still unclear.
View Article and Find Full Text PDFActivation of platelets and the complement system in mice with -induced pulmonary hypertension.
Am J Physiol Lung Cell Mol Physiol
November 2024
Section of Neonatology, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States.
Schistosomiasis-induced pulmonary hypertension (PH) presents a significant global health burden, yet the underlying mechanisms remain poorly understood. Here, we investigate the involvement of platelets and the complement system in the initiation events leading to -induced PH. We demonstrate that exposure leads to thrombocytopenia, platelet accumulation in the lung, and platelet activation.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!