Thyroid disturbance related to chronic hepatitis C infection: role of CXCL10
Débora Lucia Seguro DanilovicMaria Cássia Mendes-CorrêaMaria Cristina ChammasHéverton ZambriniRaffaelle Kasprowicz BarrosSuemi Marui
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Abstract:
Association between autoimmune thyroid diseases (AITD) and hepatitis C is controversial, but may occur or worsen during alpha-interferon treatment. The mechanism responsible for autoimmune diseases in infected patients has not been fully elucidated. This study aims to evaluate the frequency of AITD in chronic hepatitis C and the association of chemokine (CXC motif) ligand 10 (CXCL10) and AITD. One hundred and three patients with chronic hepatitis C and 96 controls were prospectively selected to clinical, hormonal, thyroid autoimmunity and ultrasound exams, besides thyroxine-binding globulin (TBG) and CXCL10 measurements and hepatic biopsies. The frequency of AITD among infected subjects was similar to controls. TT3 and TT4 distributions were right shifted, as was TBG, which correlated to both of them. Thyroid heterogeneity and hypoechogenicity were associated with AITD. Increased vascularization was more prevalent in chronic hepatitis C.CXCL10 was higher in infected patients (p=0.007) but was not related to thyroid dysfunction. Increase in CXCL10 levels were consistent with hepatic necroinflammatory activity (p=0.011). In summary, no association was found between chronic hepatitis C and AITD. Infected subjects had higher TT3 and TT4 which were correlated to TBG. Increased CXCL10 was not associated to thyroid dysfunction in HCV-infected population.Keywords:
Viral Hepatitis
Hepatitis C
Autoimmune Hepatitis
CXCL11
CXCL16
CXCL9
CCR4
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Human rhinovirus (HRV) infections induce epithelial cell production of chemokines that may contribute to the pathogenesis of exacerbations of chronic obstructive pulmonary disease (COPD) and asthma. Cigarette smoking is the predominant risk factor for the development of COPD and also aggravates asthma symptoms. We examined whether cigarette smoke extract (CSE) modulates viral inflammation by altering the profile of HRV-induced epithelial chemokine production. Purified HRV-16, and CSE were used to examine the effects on CXC chemokine ligand (CXCL)8 and CXCL10 production from both primary human bronchial epithelial cells and the BEAS-2B epithelial cell line. Both CSE and HRV-16 induced CXCL8 production and, when used in combination, induced at least an additive production of CXCL8 compared with either stimulus alone. In contrast, CSE did not induce CXCL10 and markedly inhibited HRV-16-induced CXCL10 production. Inhibition of HRV-16-induced CXCL10 by CSE was mediated, at least in part, via transcriptional regulation. The increased CXCL8 production seen with the combination of CSE and HRV-16 was not due to transcriptional regulation but was associated with CXCL8 mRNA stabilisation. Thus, CSE differentially modulates HRV-16-induced chemokine production from human airway epithelial cells in a manner that might be expected to alter inflammatory cell profiles.
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Interleukin 8
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In the article, on the example of a clinical case, a variant of the course of severe acute autoimmune hepatitis type II in a 20-year-old woman is analyzed. The prevalence of this disease are presented. Possible types of autoimmune hepatitis course are discussed. The main diagnostic criteria that indicate the likelihood of autoimmune hepatitis and the tactics of managing these patients are described.
This clinical case demonstrates that in the absence of epidemiological, anamnestic data indicating a possible viral or toxic liver damage, it is necessary to think and exclude autoimmune liver damage. It is believed that the level of gamma globulin exceeding more than 1.5 times the upper limit of normal and the absence of viral hepatitis are independent predictors of the presence of autoimmune hepatitis, and the earlier immunosuppressive therapy is started, the more favorable the prognosis of the disease.
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Viral Hepatitis
Hepatitis C
Liver disease
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Problem statement: Dysbalance of T-helper-cell (Th) cytokines and chemokines was suggested to contribute to the pathogenesis of Systemic Lupus Erythematosus (SLE). Recent reports suggest the involvement of cytokines and chemokines in the pathogenesis of SLE, but their relationship with each other and particularly in the severity of disease, was not yet understood. We analyzed the interaction between cytokines and chemokines and their relationship with severity of disease in SLE. Approach: Serum levels of cytokines and chemokines were determined by ELISA and severity of disease were measured by by using SLE Disease Activity Index (SLEDAI) score. Results: The serum levels of cytokine (IL-2, IFN-γ, IL-6, IL-10 and IL-12) and chemokine (CCL2, CCL5 and CXCL10) were variably associated with disease activity in SLE patients. Strict interaction between cytokines and chemokines was observed in SLE patients. Interleukin-6 was positively correlated with CCL5 while IL-12 was also analogous correlated with CXCL10 in SLE patients. The kidney involvement in SLE patients was related with intense increased levels of cytokines (IFN-γ, IL-12) and chemokines (CCL2, CCL5 and CXCL10). Conclusion: These data suggest that interplay of cytokines and chemokines may be involved in the severity of disease. Also, a better understanding of the cytokines and chemokines interaction may likely to provide important clues to the pathogenic mechanism and pave the way toward more effective therapeutics.
Pathogenesis
CCL5
CX3CL1
Proinflammatory cytokine
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CXCL9
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CXCL11
CXCL9
CCL3
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Chemokine research offers insightful information on the pathogenesis of cutaneous immune disorders, such as vitiligo. Compared to cytokines, the higher detectable levels of chemokines display promising potential as future disease biomarkers. Nonetheless, some published study results are contradictory, which can be attributed to patient characteristics and methodological differences. In this study, a meta-analysis was performed to compare chemokine expression in blood and skin samples from vitiligo patients versus healthy controls. Furthermore, the relationship between chemokine expression and disease activity was evaluated. Chemokine levels were investigated in 15 articles in the circulation and in 9 articles in vitiligo skin. Overall, some clear trends were observed. CXCR3 signaling by CXCL10 and CXCL9 has been confirmed by several reports, although CXCL10 showed more robust findings in blood samples. In this meta-analysis, CCL5, CXCL8, CXCL12, and CXCL16 levels were also significantly elevated. This indicates a complex immune pathway activation in vitiligo that overall supports a Th1-dominant response. Chemokines linked to the Th2 and Th17 pathways were less prevalent. Despite these findings, study protocols that examine a broader range of chemokines are encouraged, because current research is mostly focused on a small number of chemokines that were differentially expressed in previous studies.
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CXCL9
CCL5
CXCR3
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1030 www.thelancet.com Vol 388 September 10, 2016 A recurring question about viral hepatitis is why it receives so little funding and attention from global health policy makers and donors. For example, the Sustainable Development Goals have a goal to “end the epidemics of” HIV, tuberculosis, and malaria by 2030 while only “combating” hepatitis, despite the fact that hepatitis accounts for more deaths than each of those infections individually. One reason for this is the diffi culty in accurately quantifying and explaining the morbidity and mortality related to viral hepatitis. This diffi culty stems from the fact that hepatitis deaths are caused by fi ve distinct viruses (hepatitis A–E) with diff erent routes of transmission, that death occurs decades after infection, and that when people die with hepatitis-related liver cancer and cirrhosis, these deaths are not always linked to the underlying infection. In The Lancet, Jeff rey Stanaway and colleagues have made a major advance in addressing these challenges. Using the Global Burden of Disease (GBD) Study approach, which estimates the causes of mortality and morbidity and their relative importance, they have assessed the burden of disease caused by viral hepatitis from 1990 to 2013 at the country, regional, and global levels. The main conclusion from their analysis is that viral hepatitis accounted for 1·45 million deaths (95% uncertainty interval [UI] 1·38–1·54) in 2013, a 63% (95% UI 52–75) increase compared with the 0·89 million deaths (0·86–0·94) in 1990. Morbidity also increased in terms of years lived with disability (from 0·65 million [0·45–0·89] to 0·87 million [0·61–1·18]) and disability-adjusted life-years (DALYs; from 31·7 million [30·2–33·3] to 42·5 million [39·9–45·6]). The biggest increase was noted for hepatitis C infection, for which the rate of DALYs increased by 43%. Most The global burden of viral hepatitis: better estimates to guide hepatitis elimination eff orts balloon assisted maturation is not done in these centres. However, the low patency rate does raise the question of whether the benefi t of BPB would still be evident at higher patency rates. The study results seem to suggest that sympathetic blockade with BPB is of sustained benefi t in patients undergoing radiocephalic fi stula formation, and both surgeons and anaesthetists should consider its use in this group of patients.
Viral Hepatitis
Hepatitis C
Global Health
Hepatitis B
Hepatitis E
Liver disease
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Monocyte
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Chemokines recruit and activate leukocytes, assisting granuloma formation. Herein, we evaluated plasma chemokines in patients with active tuberculosis (ATB) and after completing treatment (TTB) and compared them to BCG-vaccinated healthy controls (HC). Levels of chemokines were measured by cytometric bead array. Levels of CXCL8, CXCL9 and CXCL10 were higher in ATB patients compared to HC, but they decreased in TTB. Levels of CCL2 and CCL5 in ATB patients were similar to those observed in HC. Thus, the high levels of CXC-chemokines detected during ATB, which can modulate the trafficking of immune cells from the periphery to the site of infection, were reversed by anti-mycobacterial treatment.
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Interleukin 8
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