CXCL16 contributes to neutrophil recruitment to cerebrospinal fluid in pneumococcal meningitis.

In this study, we analyzed the expression and function of CXCL16 in pneumococcal meningitis. CXCL16 was found to be up‐regulated in RAW264.7 macrophages (but not in neutrophils and endothelial cells) upon pneumococcal stimulation, in the cerebrospinal fluid of patients, and in the brains as well as the cerebrospinal fluid of mice with pneumococcal meningitis.

The chemokine CXCL13 is a key regulator of B cell recruitment to the cerebrospinal fluid in acute Lyme neuroborreliosis.

Background: The chemokine CXCL13 is known to dictate homing and motility of B cells in lymphoid tissue and has been implicated in the formation of ectopic lymphoid tissue in chronic inflammation. Whether it influences B cell trafficking during acute infection, is largely unclear. In previous studies, we showed that (I) CXCL13 levels are markedly increased in the B cell-rich cerebrospinal fluid (CSF) of patients with acute Lyme neuroborreliosis (LNB), and (II) CXCL13 is released by monocytes upon recognition of borrelial outer surface proteins by Toll-like receptor 2.

The chemokine CXCL13 in acute neuroborreliosis.

Objective: Recent studies have suggested an important role of the B cell chemoattractant CXCL13 in acute neuroborreliosis (NB). Our aim was to confirm the diagnostic role of CXCL13 and to evaluate its relevance as a therapy response and disease activity marker in NB.

Methods: CXCL13 was measured in cerebrospinal fluid (CSF) and serum of patients with NB (n=28), systemic borreliosis (SB, n=9), Guillain-Barré syndrome (GBS, n=11), Bell's palsy (BP, n=19), other cranial nerve palsies (CNP, n=5), cephalgia (C, n=20), bacterial CNS infections (B-CNS-I, n=16) and viral CNS infections (V-CNS-I, n=18).

Clonally expanded plasma cells in the cerebrospinal fluid of patients with central nervous system autoimmune demyelination produce "oligoclonal bands".

Clonally expanded plasma cells (cePC) and oligoclonal IgG (oligoclonal bands, OCB) in the cerebrospinal fluid (CSF) suggest an involvement of B cell mechanisms in autoimmune CNS demyelination. Due to their CSF-restricted occurrence, OCB are commonly believed to be the products of B cells inside the borders of the blood brain barrier. A comparison of CSF cell Ig transcriptomes and CSF-Ig proteomes recently demonstrated, that in multiple sclerosis patients CSF cells are the origin of CSF immunoglobulins.

What are the indications for lumbar puncture in patients with Lyme disease?

Lyme neuroborreliosis (LNB) is a tick-borne disease of the nervous system, caused by the spirochete Borrelia burgdorferi. Having entered the host at the site of the tick bite, the spirochetes can initially cause a local inflammatory reaction, called erythema migrans. If left untreated, the Borrelia can disseminate in the second stage of the disease and invade the central nervous system, causing LNB.

Autoimmune-mediated polyneuropathy triggered by borrelial infection?

A patient with proven borrelial infection of the central nervous system (CNS) and progressive weakness of the arms was treated with antibiotics. Although the initially elevated CXCL13 concentration in the cerebrospinal fluid decreased, indicating effective treatment of the infection, weakness progressed. Investigation revealed multiple nerve conduction blocks and the presence of GM1 antibodies, suggesting a multifocal motor neuropathy; the patient improved on treatment with intravenous immunoglobulins.

The pathogenesis of lyme neuroborreliosis: from infection to inflammation.

This review describes the current knowledge of the pathogenesis of acute Lyme neuroborreliosis (LNB), from invasion to inflammation of the central nervous system. Borrelia burgdorferi (B.b.

Borrelia garinii induces CXCL13 production in human monocytes through Toll-like receptor 2.

Recent studies have suggested an important role for the B-cell-attracting chemokine CXCL13 in the B-cell-dominated cerebrospinal fluid (CSF) infiltrate in patients with neuroborreliosis (NB). High levels of CXCL13 were present in the CSF of NB patients. It has not been clear, however, whether high CSF CXCL13 titers are specific for NB or are a characteristic of other spirochetal diseases as well.

Complement C1q and C3 are critical for the innate immune response to Streptococcus pneumoniae in the central nervous system.

Previous studies suggest that the complement system can contribute to limiting pneumococcal outgrowth within the CNS. In this study, we evaluated the role of the complement system in the activation of the innate immune response and the development of the prognosis-relevant intracranial complications in a murine model of pneumococcal meningitis. Thereby, we used mice deficient in C1q, lacking only the classical pathway, and C3, lacking all three complement activation pathways.

Adhesion of Borrelia garinii to neuronal cells is mediated by the interaction of OspA with proteoglycans.

To study pathogenic mechanisms of Lyme meningoradiculitis, dorsal root ganglia (DRG) cells and two neuronal cell lines (B50, SH-SY5Y) were incubated with Borrelia garinii, the Borrelia species most frequently isolated from CSF of Lyme neuroborreliosis patients in Europe. We demonstrated that (I) OspA-positive B. garinii adhere to neuronal cells, (II) Borrelia adhesion can be blocked by a monoclonal antibody against OspA, (III) preincubation with proteoglycans interferes with the adhesion process and (IV) rOspA directly binds to the proteoglycans.

Clinical aspects of neuroborreliosis and post-Lyme disease syndrome in adult patients.

The diagnostic criteria of active neuroborreliosis include inflammatory changes of the cerebrospinal fluid (CSF) and an elevated specific Borrelia CSF-to-serum antibody index, indicating intrathecal Borrelia antibody production. Patients with neuroborreliosis are usually treated with intravenous ceftriaxone for 2-3 weeks. In case of allergy, doxycycline may be used.

CXCL11 is involved in leucocyte recruitment to the central nervous system in neuroborreliosis.

We investigated the role of the CXCR3 chemokine CXCL11 (I-TAC) for leukocyte recruitment to the CSF in neuroborreliosis (NB). CXCL11 levels in the CSF of 17 patients with acute NB were elevated compared with 20 non-inflammatory controls (100.1 vs.

Severe meningoencephalitis caused by human herpesvirus 6 type B in an immunocompetent woman treated with ganciclovir.

Human herpesvirus 6 (HHV-6), the causative agent of exanthema subitum in childhood, can also induce meningoencephalitis in immunocompromised individuals. In contrast, HHV-6 encephalitis in immunocompetent patients is rare, and the clinical syndrome not well defined. We report a case of meningoencephalitis caused by HHV-6 type B in an otherwise healthy woman.

Successful cardic surgery 24 hours after craniotomy in a patient with infective endocarditis and embolic cerebellar infarction: case report.

Follow up management in a patient already treated with decompressive craniotomy for a space-occupying endocarditic stroke is difficult. While immediate valve replacement eliminates the focus and therefore the high risk of re-embolization, a neurosurgical intervention is considered a contraindication to early cardiosurgery. Herein, the first report is presented of a critically ill patient with bacterial endocarditis and a space-occupying cerebellar infarction with imminent herniation, who successfully underwent mitral valve replacement only 24 h after decompressive craniotomy.