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Review
, 2016, 8413768

IL-32: A Novel Pluripotent Inflammatory Interleukin, Towards Gastric Inflammation, Gastric Cancer, and Chronic Rhino Sinusitis

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Review

IL-32: A Novel Pluripotent Inflammatory Interleukin, Towards Gastric Inflammation, Gastric Cancer, and Chronic Rhino Sinusitis

Muhammad Babar Khawar et al. Mediators Inflamm.

Abstract

A vast variety of nonstructural proteins have been studied for their key roles and involvement in a number of biological phenomenona. Interleukin-32 is a novel cytokine whose presence has been confirmed in most of the mammals except rodents. The IL-32 gene was identified on human chromosome 16 p13.3. The gene has eight exons and nine splice variants, namely, IL-32α, IL-32β, IL-32γ, IL-32δ, IL-32ε, IL-32ζ, IL-32η, IL-32θ, and IL-32s. It was found to induce the expression of various inflammatory cytokines including TNF-α, IL-6, and IL-1β as well as macrophage inflammatory protein-2 (MIP-2) and has been reported previously to be involved in the pathogenesis and progression of a number of inflammatory disorders, namely, inflammatory bowel disease (IBD), gastric inflammation and cancer, rheumatoid arthritis, and chronic obstructive pulmonary disease (COPD). In the current review, we have highlighted the involvement of IL-32 in gastric cancer, gastric inflammation, and chronic rhinosinusitis. We have also tried to explore various mechanisms suspected to induce the expression of this extraordinary cytokine as well as various mechanisms of action employed by IL-32 during the mediation and progression of the above said problems.

Figures

Figure 1
Figure 1
Mechanism of synthesis of IL-32 by different body cells (T-cells, epithelial cells, and blood monocytes) induced by various cytokines. IL-32 after its secretion affects a number of biological activities, namely, apoptosis and cell differentiation as well as mediation of inflammation.
Figure 2
Figure 2
How gastric cancerous cells lead to inflammation mediated by IL-32. Infections in the body set in motion the synthesis and secretion of a variety of proinflammatory and inflammatory cytokines which results in the development of tumor microenvironment in gastric cancerous cells that are continuously involved in the production of IL-8 which exerts its biological influence by initiating the production of IL-32 which is blamed to be involved in gastric inflammation.
Figure 3
Figure 3
Microbial infection induced expression of IL-32 results in gastric inflammation. Microbial infection (H. pylori) leads to the upregulation of cagPAI cluster of genes which through the activation of NF-κB pathway results in the synthesis of IL-32 and some other potent inflammatory cytokines (IL-1, IL-8, and TNF-α) that results in gastric inflammation. The resulting inflammation self-augments the activation of NF-κB pathway which further aggravates the situation.
Figure 4
Figure 4
Involvement of Staphylococcus aureus in IL-32 induced inflammation in chronic rhinosinusitis. Staphylococcus aureus induces the expression of IL-32 as well as initiating the NOD-dependent pathway and TLR-dependent pathway which synergistically stimulate the production of some potent proinflammatory cytokines that results in inflammation of chronic rhinosinusitis.

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