Regulated Production of CXCL13 within the Central Nervous System

Irani, David N.

doi:10.4172/2155-9899.1000460

Cited by 36 publications

(41 citation statements)

References 82 publications

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“…With this study, we provide evidence that CXCL13 does not enter CSF from blood, a finding of high relevance regarding the potential of CSF CXCL13 as diagnostic, prognostic, severity, and treatment response marker for neuroinflammatory conditions such as LNB, CNS lymphoma, demyelinating CNS diseases, and neuroinfections, and regarding a potential caveat when calculating CSF/serum CXCL13 quotients [8,[18][19][20]29].…”

Section: Discussionmentioning

confidence: 84%

“…CXCL13 also occurs in CNS inflammation and is the focus of biomarker research for Lyme neuroborreliosis (LNB), CNS lymphoma, and multiple sclerosis (MS) [8]. The broad spectrum of CNS inflammatory conditions with CXCL13 elevations in CSF also include bacterial/ viral and aseptic meningitis, encephalitis, myelitis, and autoimmune encephalitis [9][10][11][12][13][14].…”

Section: Open Accessmentioning

confidence: 99%

“…The function of CSF CXCL13 is only partly established and mainly attributed to B cell chemoattraction to the CNS [15]. The pathogenic relevance is associated with B cell-related immune activation during acute and active neuroinflammation [8]. It is proposed, that the CNS source for CXCL13 are monocytes in LNB, lesion infiltrating macrophages, perivascular stromal cells in primary CNS lymphoma, microglia or meningeal TLS cells in MS [15][16][17].…”

Section: Open Accessmentioning

confidence: 99%

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Chemokine CXCL13 in serum, CSF and blood–CSF barrier function: evidence of compartment restriction

Pilz

Sakic

Wipfler

et al. 2020

Fluids Barriers CNS

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Background and purpose: Elevation of the chemokine CXCL13 in CSF frequently occurs during active and acute CNS inflammatory processes and presumably is associated with B cell-related immune activation. Elevation levels, however, vary a lot and "leaking" of CXCL13 from blood across dysfunctional brain barriers is a possible source. The aim was to clarify the relation between CXCL13 concentrations in CSF, CXCL13 concentrations in serum and blood-CSF barrier (BCSFB) function for a correct interpretation of the intrathecal origin of CXCL13. Methods: We retrospectively analyzed CXCL13 of banked CSF/serum samples (n = 69) selected from patient records and categorized the CSF CXCL13 elevations as CXCL13 negative (< 30 pg/ml), low (30-100 pg/ml), medium (101-250 pg/ml), or high (> 250 pg/ml). CXCL13 concentrations in CSF and serum and the corresponding CSF/serum CXCL13 quotients (Qcxcl13) were compared to CSF/serum albumin quotients (QAlb) as a measure for BCSFB function. The CXCL13 negative category included two subgroups with normal and dysfunctional BCSFB. Results: Serum CXCL13 concentrations were similar across categories with median levels around 100 pg/ml but differed between individuals (29 to > 505 pg/ml). Despite clear evidence in serum, CXCL13 was detectable only at trace amounts (medians 3.5 and 7.5 pg/ml) in CSF of the two CXCL13 negative subgroups irrespective of a normal or pathological QAlb. Moreover, we found no association between CSF and serum CXCL13 levels or between QAlb and CSF CXCL13 levels in any of the CSF CXCL13-delineated categories. CXCL13 apparently does not "leak" from blood into CSF. This implies an intrathecal origin also for low CSF CXCL13 levels and a caveat for analyzing the Qcxcl13, because higher serum than CSF concentrations arithmetically depress the Qcxcl13 resulting in misleadingly low CSF/serum quotients. Conclusion: We demonstrated that CXCL13 does not cross from blood into CSF, not even during severe BCSFB dysfunction. CSF CXCL13 elevations therefore most likely always are CNS-derived, which highlights their relevance as indicator of inflammatory CNS processes. We recommend data should not be corrected for BCSFB permeability (QAlb) and not to calculate CSF/serum quotients for CXCL13 as these may introduce error.

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Section: Discussionmentioning

confidence: 84%

Section: Open Accessmentioning

confidence: 99%

Section: Open Accessmentioning

confidence: 99%

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Chemokine CXCL13 in serum, CSF and blood–CSF barrier function: evidence of compartment restriction

Pilz

Sakic

Wipfler

et al. 2020

Fluids Barriers CNS

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“…After binding to the G-protein receptor CXCR5 on neutrophils and mast cells, CXCL13 elicits chemotaxis and migration of B lymphocytes from lymphoid tissues to the site of inflammation. Importantly, it has been suggested that CXCL13 is involved in neurological damage through promoting B cell migration to the CSF and activating them, subsequently leading to CSF pleocytosis with characteristic B cell elevation [12,13,[22][23][24][25][26]. Therefore, the aim of this study was to conduct a review of the current literature regarding CXCL13 in serum and CSF to determine its diagnostic significance in spirochetal neurological diseases neuroborreliosis and neurosyphilis.…”

Section: Introductionmentioning

confidence: 99%

Chemokine Ligand 13 (CXCL13) in Neuroborreliosis and Neurosyphilis as Selected Spirochetal Neurological Diseases: A Review of Its Diagnostic Significance

Gudowska-Sawczuk

Mroczko

2020

IJMS

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Neuroborreliosis (NB) and neurosyphilis (NS) are abnormal conditions caused by spirochetal bacteria which affect the nervous system. Diagnosis of neuroborreliosis and neurosyphilis is determined by clinical examination of visible symptoms, serum and cerebrospinal fluid (CSF) analysis, and serological detection of antibodies against Borrelia burgdorferi sensu lato and Treponema pallidum, respectively. Establishing a diagnosis may sometimes pose a number of diagnostic difficulties. A potential role of chemokine ligand 13 (CXCL13) as an accurate diagnostic biomarker of intrathecal inflammation has been suggested. In this review, we focused on changes in serum and cerebrospinal fluid concentration of chemokine ligand 13 in selected spirochetal neurological diseases neuroborreliosis and neurosyphilis reported in the available literature. We performed an extensive search of the literature relevant to our investigation via the MEDLINE/PubMed database. It has been proven that CXCL13 determination can provide rapid information regarding central nervous system inflammation in patients with selected spirochetosis. We described that neuroborreliosis and neurosyphilis are associated with an elevated CXCL13 concentration, mainly in the cerebrospinal fluid. Moreover, literature data suggest that CXCL13 determination is the most interesting additional marker for diagnosis and monitoring of neuroborreliosis and neurosyphilis thanks to its high sensitivity. Based on these published findings, we suggest that CXCL13 has high diagnostic utility and may be applied in laboratory diagnostics as a potential diagnostic marker in human spirochetal neurologic diseases.

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“…CXC ligand 13 (CXCL13) is a main factor for recruiting B cells in neuro-inflammatory reaction. In various inflammatory diseases, a large number of monocytes aggregate, and chemokine CXCL13 is expressed in a large amount locally, further leading to inflammatory cascade reaction and local tissue or organ damage (9)(10)(11). IL-6, as a very important part of interleukins, and participates in many inflammatory reactions and diseases in human body (12,13).…”

Section: Introductionmentioning

confidence: 99%

Changes in expression of serum chemokine CXCL13 and IL-6 after hip replacement, and the relationship with lower limb vein thrombus

Guan

2019

Exp Ther Med

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Changes in the expression of serum chemokine CXC ligand 13 (CXCL13) and interleukin-6 (IL-6), and the relationship with lower limb vein thrombus were explored. A total of 128 patients undergoing hip replacement in The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine from May 2017 to June 2019 were selected, and the patients suffering from lower limb vein thrombus were enrolled as group A and other patients not suffering from it were enrolled as group B. Enzyme-linked immunosorbent assay was employed to determine the levels of serum chemokine CXCL13 and IL-6, and receiver operating characteristic curves of serum chemokine CXCL13 and IL-6 levels in diagnosing restenosis after surgery were drawn. Pearson's correlation coefficient was adopted to analyze the correlation between serum chemokine CXCL13 and IL-6, and the logistic regression analysis to analyze the risk factors affecting hip replacement in patients. The levels of serum CXCL13 and IL-6 in group A were significantly higher than those in group B (both P<0.001). The specificity and sensitivity of serum CXCL13 level in diagnosis of lower limb vein thrombus after hip replacement were 61.76 and 80.00%, respectively, and those of serum IL-6 level in diagnosis were 70.59 and 66.67%, respectively. Serum CXCL13 level was positively correlated with serum IL-6 level (P<0.001), and age, body mass index (BMI), CXCL13 level and IL-6 level of the patients were independent risk factors affecting the efficacy of hip replacement. Serum CXCL13 level and serum IL-6 level can be used as biological indexes for prediction of early lower limb vein thrombus after hip replacement, and logistic regression analysis revealed that the age of the patients, BMI, diabetes history, hyperlipidemia history, hypertension history, CXCL13 level and IL-6 level are independent risk factors affecting the efficacy of hip replacement.

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Regulated Production of CXCL13 within the Central Nervous System

Cited by 36 publications

References 82 publications

Chemokine CXCL13 in serum, CSF and blood–CSF barrier function: evidence of compartment restriction

Chemokine CXCL13 in serum, CSF and blood–CSF barrier function: evidence of compartment restriction

Chemokine Ligand 13 (CXCL13) in Neuroborreliosis and Neurosyphilis as Selected Spirochetal Neurological Diseases: A Review of Its Diagnostic Significance

Changes in expression of serum chemokine CXCL13 and IL-6 after hip replacement, and the relationship with lower limb vein thrombus

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