Eosinophils Chemoattracted by Eotaxin from Cerebrospinal Fluid of Mice Infected with <i>Angiostrongylus Cantonensis</i> Assayed in a Microchamber

Chang, Eddy Essen; Yen, Chuan-Min

doi:10.1016/s1607-551x(09)70108-1

Cited by 11 publications

(14 citation statements)

References 23 publications

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“…Although increased CSF CCL11 and CXCL10 levels in ME/CFS subjects, along with dysregulation of IL1 signaling, suggest the possibility of an allergic process in central compartments, 49,50 such patterns may also be seen in a wide range of CNS infections. [51][52][53][54] Additional studies focused on delineating the relationships of clinical phenotypes of ME/CFS to immune profiles in both the CSF and the peripheral blood are of paramount importance to investigating potential causes and biomarkers for disease. Recent reports indicate regional changes in white matter volume 19 and abnormalities in myelin in white matter tracts in ME/CFS.…”

Section: Discussionmentioning

confidence: 99%

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

et al. 2015

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Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.

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Section: Discussionmentioning

confidence: 99%

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

et al. 2015

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“…Finally, BBB disruption during eosinophilic meningitis involves a complex interaction between eosinophils and mediators, such as interleukin-4, interleukin-5, platelet-activating factor, nitric oxide, and matrix metalloproteinases, which might induce BBB permeability, independent of HGF. 9,[28][29][30] In conclusion, we found that patients with eosinophilic meningitis had elevated HGF levels in the CSF. The clinical significance needs to be clarified further.…”

mentioning

confidence: 48%

Dynamic Changes of Hepatocyte Growth Factor in Eosinophilic Meningitis Caused by Angiostrongylus cantonensis Infection

Tsai

Huang

Liu

et al. 2009

The American Journal of Tropical Medicine and Hygiene

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Hepatocyte growth factor (HGF) is a member of the angiogenic growth factor family, which exerts a variety of effects on epithelial, endothelial, and neuronal cells by binding to the c-MET receptor tyrosine kinase. It was reported that HGF attenuates cerebral ischemia-induced increase in permeability of the blood-brain barrier (BBB) and decreases in expression of tight junction proteins in cerebral vessels of rats. Studies on the localization of the c-Met/HGF receptor in the rat brain and the interaction with HGF after brain injuries show that HGF plays an important role as a neurotrophic factor in the brain. To assess the role of HGF in patients with eosinophilic meningitis, a retrospective, cohort study was conducted to measure the dynamic changes of HGF in the cerebrospinal fluid (CSF) and blood of nine patients with eosinophilic meningitis. The mean HGF(CSF) at presentation, 1 week, 2 weeks, and 3 weeks after admission was 539 pg/mL, 540 pg/mL, 376 pg/mL, and 279 pg/mL, respectively. The mean level of HGF(CSF) at presentation (539 +/- 242 pg/mL) and 1 week after admission (540 +/- 213 pg/mL) was significantly higher than in controls (162 +/- 207 pg/mL)(P = 0.02 and P = 0.01, respectively). The CSF/blood ratio of HGF at presentation (0.61) was higher when compared with physiologic situations in uninfected individuals (0.51). The levels of HGF in CSF were not correlated with the amount of CSF cells or proteins. All patients recovered without neurologic sequelae. These results indicate that high concentrations of HGF in the CSF occur in eosinophilic meningitis, and may have a role in protecting against endothelial injury and reducing BBB dysfunction.

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“…A total of 1000 cells from multiple fields were examined for each slide. Counts of total cells, eosinophils, macrophage, neutrophils, and lymphocytes were performed on blinded samples, as described previously [69].…”

Section: Bronchoalveolar Lavage Collection and Cell Countingmentioning

confidence: 99%

Allergen specific Treg upregulated by lung-stage schistosome infection alleviates allergic airway inflammation via inhibiting IgE secretion

Zhang

Luo

et al. 2020

Preprint

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Schistosome infection showed protective effects against allergic airway inflammation (AAI). However,controversial findings exist especially regarding the timing of helminth infection and the underlying mechanisms. Moreover, most previous studies focused on understanding the preventive effect of schistosome infection on asthma (infection before allergen sensitization), while its therapeutic effects (infection after allergen sensitization) were rarely investigated. In this study, we investigated the therapeutic effects of schistosome infection on AAI using a mouse model of OVA induced asthma. To explore how the timing of schistosome infection influences its therapeutic effect, the mice were percutaneously infected with cercaria of Schistosoma japonicum at either 1 day before OVA induced asthma attack (infection at lung-stage during AAI) or 14 days before OVA induced asthma attack (infection at post lung-stage during AAI). We found that lung-stage schistosome infection significantly ameliorated OVA-induced AAI, whereas post lung-stage infection showed no therapeutic effect. Mechanistically, the lung-stage schistosome infection significantly upregulated the frequency of Treg, especially OVA specific Treg, in lung tissue, which negatively correlated with the level of OVA specific IgE. Depletion of Treg in vivo counteracted the therapeutic effect. Furthermore, transcriptomic analysis of lung tissue showed that lung-stage schistosome infection during AAI shaped the microenvironment to favor Treg induction. In conclusion, our data showed that lung-stage schistosome infection could relieve OVA induced asthma in a mouse model. The therapeutic effect was mediated by the upregulated OVA specific Treg which suppressed IgE production and Th2 cytokine secretion. Our results may facilitate the discovery of a new therapy for AAI.

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Eosinophils Chemoattracted by Eotaxin from Cerebrospinal Fluid of Mice Infected with Angiostrongylus Cantonensis Assayed in a Microchamber

Cited by 11 publications

References 23 publications

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

Dynamic Changes of Hepatocyte Growth Factor in Eosinophilic Meningitis Caused by Angiostrongylus cantonensis Infection

Allergen specific Treg upregulated by lung-stage schistosome infection alleviates allergic airway inflammation via inhibiting IgE secretion

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