Role of interleukin-22 in tuberculosis patients.
interleukin-22
mycobacterium
tuberculosis
Journal
Journal of basic and clinical physiology and pharmacology
ISSN: 2191-0286
Titre abrégé: J Basic Clin Physiol Pharmacol
Pays: Germany
ID NLM: 9101750
Informations de publication
Date de publication:
01 Jan 2023
01 Jan 2023
Historique:
received:
28
04
2022
accepted:
21
09
2022
pubmed:
15
10
2022
medline:
27
1
2023
entrez:
14
10
2022
Statut:
epublish
Résumé
Disease progression of tuberculosis (TB) depends on the balance between the microorganism's virulence and the host defense systems (mainly T cell-mediated immune response). Interleukin-22 (IL-22) helps in cell proliferation and regeneration and provides protection against microbial diseases. The IL-22-producing T cells can migrate into the granulomas during TB infection. However, disparity exists in literature regarding its role. The present study aims to compare serum IL-22 levels and its' expression in TB patients and healthy controls. 87 TB patients and 85 healthy subjects were enrolled in the study. Under aseptic conditions, venous blood was withdrawn. Serum IL-22 levels were estimated using enzyme-linked immunosorbent assay, and its gene expression was assessed using SYBR green-based quantitative PCR technology. A statistical analysis was performed using SPSS. The median (interquartile range) of serum IL-22 levels was significantly lower in TB patients (18.55 (5.08) pg/mL) when compared to controls (49.38 (162.88) pg/mL) (p<0.0001). The IL-22 expression was significantly upregulated with a fold change value of 29.44 in TB patients. The IL-22 levels were found to be significantly decreased in patients, contradictory to its expression, which is upregulated. It plays a crucial role for the modulation of tissues in response to TB infection.
Identifiants
pubmed: 36239667
pii: jbcpp-2022-0106
doi: 10.1515/jbcpp-2022-0106
doi:
Substances chimiques
Interleukins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
83-89Informations de copyright
© 2022 Walter de Gruyter GmbH, Berlin/Boston.
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