Dataset Information

Case Report: Analysis of Inflammatory Cytokines IL-6, CCL2/MCP1, CCL5/RANTES, CXCL9/MIG, and CXCL10/IP10 in a Cystic Fibrosis Patient Cohort During the First Wave of the COVID-19 Pandemic.

ABSTRACT: Since the beginning of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, data registered in the European countries revealed increasing cases of infection in cystic fibrosis (CF) patients. In the course of this pandemic, we enrolled 17 CF patients for a study evaluating inflammatory markers. One of them developed COVID-19, giving us the possibility to analyze inflammatory markers in the acute phase as compared to levels detected before and after the infectious episode and to levels measured in the other CF patients enrolled to the study who did not experience COVID-19 and 23 patients referred to our center for SARS-CoV-2 infection.

SUBMITTER: Baresi G

PROVIDER: S-EPMC8291286 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature

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Case Report: Analysis of Inflammatory Cytokines IL-6, CCL2/MCP1, CCL5/RANTES, CXCL9/MIG, and CXCL10/IP10 in a Cystic Fibrosis Patient Cohort During the First Wave of the COVID-19 Pandemic.

Baresi Giulia G Giacomelli Mauro M Moratto Daniele D Chiarini Marco M Conforti Immacolata Claudia IC Padoan Rita R Poli Piercarlo P Timpano Silviana S Caldarale Francesca F Badolato Raffaele R

Frontiers in pediatrics 20210706

Since the beginning of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, data registered in the European countries revealed increasing cases of infection in cystic fibrosis (CF) patients. In the course of this pandemic, we enrolled 17 CF patients for a study evaluating inflammatory markers. One of them developed COVID<b>-</b>19, giving us the possibility to analyze inflammatory markers in the acute phase as compared to levels detected before and after the infectious epis ...[more]

PMID: 34295857

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Project description:BackgroundPatients with temporomandibular joint disorders (TMD), reactive arthritis and rheumatoid arthritis often have combined etiology of hereditary and microenvironmental factors contributing to joint pain. Multiple clinical and animal studies indicate 'double-hit' inflammatory insults can cause chronic inflammation. The first inflammatory insult primes the immune system and subsequent insults elicit amplified responses. The present 'double hit' study produced a chronic orofacial pain model in mice with genetic deletion of both TNFα receptors (TNFR1/R2-/-), investigating the main nociceptive signalling pathways in comparisons to wild type mice.MethodsAn initial inflammatory insult was given unilaterally into the temporomandibular joint (TMJ). Secondary hypersensitivity was tested on the skin over the TMJ throughout the experiment. Three weeks later after complete reversal of hypersensitivity, a second inflammatory insult was imposed on the colon. Pharmacological interventions were tested for efficacy after week 10 when hypersensitivity was chronic in TNFR1/R2-/- mice. Serum cytokines were analysed at Days 1, 14, and Week 18.ResultsThe double hit insult produced chronic hypersensitivity continuing through the 4-month experimental timeline in the absence of TNFα signalling. P2X7 and NMDA receptor antagonists temporarily attenuated chronic hypersensitivity. Serum cytokine/chemokine analysis on Day 14 when CFA induced hypersensitivity was resolved identified increased levels of pro-inflammatory cytokines CCL2, CXCL9, CXCL10, RANTES and decreased levels of anti-inflammatory cytokines IL-1ra and IL-4 in TNFR1/R2-/- compared to WT mice.ConclusionsThese data suggest a causal feed-forward signalling cascade of these little studied cytokines have the potential to cause recrudescence in this orofacial inflammatory pain model in the absence of TNFα signalling.SignificanceUsing a mouse model of chronic inflammatory temporomandibular joint disorder, we determined that absence of functional TNFR1/R2 induces aberrant inflammatory signalling caused by other increased pro-inflammatory and decreased anti-inflammatory cytokines that could serve as blood biomarkers and may predict disease progression.

Project description:BackgroundNon-small cell lung cancer (NSCLC) is the most common type of lung cancer. Tumor treating fields (TTFields) combined with anti-PD immunotherapy offers a promising strategy to address this issue. Nevertheless, the mechanism of action (MOA) of TTFields therapy combined with anti-PD immunotherapy in NSCLC has not been thoroughly investigated. This study aims to elucidate the MOA of the combined therapy from the aspect of improving the tumor immune microenvironment (TIME).MethodsUsing a mouse model of NSCLC, we tested the efficacy of TTFields therapy with anti-PD-1 and anti-PD-L1 immunotherapy. By RNA-seq, the differential genes and signaling pathways between combination therapy and anti-PD therapy groups were studied. In-vitro experiments validated the effects of TTFields on tumor cells for CD4+ T cell and CD8+ T cell infiltration, as well as the expression of tumor immunogenic death related genes and chemokines.ResultsCombining TTFields with anti-PD-1 reduced tumor weight and volume, respectively, compared to controls (p < 0.05). RNA-seq analysis revealed 1,745 differentially expressed genes (DEGs) in the combination therapy group versus controls, including upregulated immune pathways and immunogenic cell death (ICD) associated genes. Further study showed that the combination therapy resulted in increased T cell infiltration compared to anti-PD immunotherapy alone, and TTFields induced higher level expression of ATP, HMGB1, CCL2, CCL8, CXCL9, and CXCL10 and inflammatory cytokines than control group. These effects collectively contributed to the altered TIME, and finally potentiated the efficacy of anti-PD therapy.ConclusionsTTFields enhance the effectiveness of anti-PD immunotherapy by improving CD4+ T cells and CD8+ T infiltration via inducing ICD to increase CCL2/8 and CXCL9/CXCL10 expression of tumor cells. This study provides theoretical basis and new insights for evaluating the effectiveness of TTFields combined with anti-PD therapy for NSCLC.

Dataset Information

Case Report: Analysis of Inflammatory Cytokines IL-6, CCL2/MCP1, CCL5/RANTES, CXCL9/MIG, and CXCL10/IP10 in a Cystic Fibrosis Patient Cohort During the First Wave of the COVID-19 Pandemic.

Publications

Case Report: Analysis of Inflammatory Cytokines IL-6, CCL2/MCP1, CCL5/RANTES, CXCL9/MIG, and CXCL10/IP10 in a Cystic Fibrosis Patient Cohort During the First Wave of the COVID-19 Pandemic.

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