Structural Characteristics of Seven IL-32 Variants

IL-32 exists as seven mRNA transcripts that can translate into distinct individual IL-32 variants with specific protein domains. These translated protein domains of IL-32 variants code for specific functions that allow for interaction with different molecules intracellularly or extracellularly. The longest variant is IL-32γ possessing 234 amino acid residues with all 11 protein domains, while the shortest variant is IL-32α possessing 131 amino acid residues with three of the protein domains. The first domain exists in 6 variants except IL-32δ variant, which has a distinct translation initiation codon due to mRNA splicing. The last eleventh domain is common domain for all seven IL-32 variants. Numerous studies in different fields, such as inflammation, autoimmunity, pathogen infection, and cancer biology, have claimed the specific biological activity of individual IL-32 variant despite the absence of sufficient data. There are 4 additional IL-32 variants without proper transcripts. In this review, the structural characteristics of seven IL-32 transcripts are described based on the specific protein domains.

Role of IL-32 Gamma on Bone Metabolism in Autoimmune Arthritis

IL-32 acts as a pro-inflammatory cytokine by inducing the synthesis of inflammatory molecules as well as promoting the morphological changes involved in the transformation of monocytes into osteoclasts (OCs). Evaluation of the functions of IL-32 has mainly focused on its inflammatory properties, such as involvement in the pathogenesis of various autoimmune diseases. Recently, IL-32 was shown to be involved in bone metabolism, in which it promotes the differentiation and activation of OCs and plays a key role in bone resorption in inflammatory conditions. IL-32γ also regulates bone formation in conditions such as ankylosing spondylitis and osteoporosis. In this review, we summarize the results of recent studies on the role of IL-32γ in bone metabolism in inflammatory arthritis.

IL32 expression in peripheral blood CD3+ cells from myelodysplastic syndromes patients

Background: Myelodysplastic syndromes (MDS) are a heterogeneous group of disorders characterized by ineffective hematopoiesis and risk of leukemia transformation. There is evidence to suggest the participation of immune system deregulation in MDS pathogenesis. Interleukin-32 (IL-32) is a newly described multifunctional cytokine reported as an important mediator in autoimmune and inflammatory disorders. In the present study, we reported the expression of IL32 and IL32 transcript variants (α, ß, γ and δ) in peripheral blood CD3+ cells from healthy controls and MDS patients. Methods: CD3+ cells were isolated by immunomagnetic cell sorting from thirty-nine untreated MDS patients and twenty-nine healthy donors. Gene expression was evaluated by quantitative PCR. For statistical analysis, Mann­Whitney test, Kruskal-Wallis test with Dunns post test and Log-rank (Mantel-Cox) were used, as appropriate. A p value <0.05 was considered statistically significant. Results: IL32 expression and IL32 transcript variants IL32α, IL32ß, IL32γ, and IL32δ, were similar in peripheral blood CD3+ cells from healthy donors and MDS patients. Increased IL-32α expression was an independent predictor for MDS disease progression by univariate and multivariate analysis. Conclusions: We observed that IL32 expression is not differently expressed in CD3+ cells from MDS patients; nevertheless IL32α has a potential role in disease progression (AU)

Interleukin-32 Gamma as a New Face in Inflammatory Bone Diseases

Interleukin-32 (IL-32), a recently identified pro-inflammatory cytokine, is involved in the pathogenesis and progression of infections, cancer, chronic inflammation, and autoimmune disease. IL-32γ is the most active isoform in cell death and cell activation among nine distinct isoforms of IL-32. IL-32γ potentiates both osteogenic and osteoclastogenic capacities, and is critical in the coupling of bone resorption and bone formation for maintenance of bone homeostasis. IL-32γ is strongly associated with inflammatory bone disorders such as rheumatoid arthritis, ankylosing spondylitis, and osteoporosis. In this review, we summarize current research on the role of IL-32γ in inflammatory bone disorders, highlighting this cytokine as a novel target for prognostic marker and control of these diseases.

Serum inflammatory factor and cytokines in AECOPD

OBJECTIVE@#To explore the serum levels of IL-32, MMP-9,PCT and CRP in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).@*METHODS@#A total of 50 patients with AECOPD and 45 cases with acute asthma attack admitted from October 2013 to August 2014 were selected, and the serum levels of IL-32, MMP-9, PCT and CRP were determined and compaed by using Double antibody sandwich Enzyme linked immunosorbent assay, immunofluorescence double antibody sandwich assay and immunoturbidimetry assay.@*RESULTS@#Serum levels of IL-32, MMP-9, PCT and CRP were significantly higher in AECOPD group than acute asthma attack group (P<0.05). IL-32 and MMP-9 were negatively correlated with lung function. MMP-9 in AECOPD patients was increased more significantly.@*CONCLUSIONS@#Serum levels of IL-32 and MMP-9 were negatively correlated with lung function, and the worse the lung function is, the more significant the increase is.

Serum inflammatory factor and cytokines in AECOPD

Objective: To explore the serum levels of IL-32, MMP-9,PCT and CRP in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Methods: A total of 50 patients with AECOPD and 45 cases with acute asthma attack admitted from October 2013 to August 2014 were selected, and the serum levels of IL-32, MMP-9, PCT and CRP were determined and compaed by using Double antibody sandwich Enzyme linked immunosorbent assay, immunofluorescence double antibody sandwich assay and immunoturbidimetry assay. Results: Serum levels of IL-32, MMP-9, PCT and CRP were significantly higher in AECOPD group than acute asthma attack group (. P<0.05). IL-32 and MMP-9 were negatively correlated with lung function. MMP-9 in AECOPD patients was increased more significantly. Conclusions: Serum levels of IL-32 and MMP-9 were negatively correlated with lung function, and the worse the lung function is, the more significant the increase is.