Liver expression of IL-22, IL-22R1 and IL-22BP in patients with chronic hepatitis C with different fibrosis stages.
Autor: | de Brito RJVC; Postgraduate program in Health Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil; College of Medicine, Federal University of the São Francisco Valley (UNIVASF), Petrolina, Pernambuco, Brazil., do Carmo RF; College of Pharmacy, Federal University of the São Francisco Valley (UNIVASF), Petrolina, Pernambuco, Brazil. Electronic address: rodrigo.carmo@univasf.edu.br., Silva BMS; College of Pharmacy, Federal University of the São Francisco Valley (UNIVASF), Petrolina, Pernambuco, Brazil., Costa ACS; Institute of Biological Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil., Rocha SWS; Postgraduate program in Health Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil; Institute of Biological Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil., Vasconcelos LRS; Department of Parasitology, Aggeu Magalhães Institute (IAM/FIOCRUZ), Recife, Pernambuco, Brazil., Pereira LMMB; Postgraduate program in Health Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil; Faculty of Medicine, University of Pernambuco (UPE), Recife, Pernambuco, Brazil; Liver Institute of Pernambuco (IFP), Recife, Pernambuco, Brazil., de Moura PMMF; Postgraduate program in Health Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil; Institute of Biological Sciences, University of Pernambuco (UPE), Recife, Pernambuco, Brazil. |
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Jazyk: | angličtina |
Zdroj: | Cytokine [Cytokine] 2022 Feb; Vol. 150, pp. 155784. Date of Electronic Publication: 2021 Dec 15. |
DOI: | 10.1016/j.cyto.2021.155784 |
Abstrakt: | Aims: Liver fibrosis is the result of an exacerbated wound-healing response associated with chronic liver injury. Interleukin-22 (IL-22) plays a key role in liver disease, through either a protective or an adverse role, depending on the context. The relationship between IL-22 and its receptors IL-22R1 and IL-22BP (soluble inhibitor) in liver fibrosis is unknown. In this study, we assessed the presence and quantity of IL-22, IL-22R1, and IL-22BP-producing cells in liver tissues of patients with chronic hepatitis C. Methods and Results: The number of IL-22-producing cells was significantly higher in stages F1, F2, and F3 when compared to F0 or F4 (p < 0.05). The immunostaining of IL-22R1 decreased as liver fibrosis increased from F1 to F4. On the other hand, the concentration of IL-22BP-producing cells was higher in patients with cirrhosis (F4). Furthermore, the IL-22BP:IL-22 ratio was highest in patients with cirrhosis. Conclusions: Our results suggest that IL-22, IL-22R1 and IL-22BP may be involved in the mechanisms of liver fibrosis in patients with chronic hepatitis C. (Copyright © 2021 Elsevier Ltd. All rights reserved.) |
Databáze: | MEDLINE |
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