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

• Published in: Mediators of inflammation Vol. 2016; no. 2016; pp. 1 - 8
• Main Authors: Khawar, Muhammad Babar, Sheikh, Nadeem, Abbasi, Muddasir Hassan
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 01.01.2016; Hindawi Limited; Wiley
• Subjects: Animals; Arthritis, Rheumatoid - immunology; Arthritis, Rheumatoid - metabolism; Chemokines; Chronic Disease; Cytokines; Development and progression; Gastric cancer; Gastritis - immunology; Gastritis - metabolism; Humans; Inflammation; Inflammatory Bowel Diseases - immunology; Inflammatory Bowel Diseases - metabolism; Interleukins; Interleukins - metabolism; Kinases; Leukemia; Molecular weight; Pathogenesis; Physiological aspects; Pulmonary Disease, Chronic Obstructive - immunology; Pulmonary Disease, Chronic Obstructive - metabolism; Review; Signal transduction; Sinusitis - immunology; Sinusitis - metabolism; Stomach cancer; Stomach Neoplasms - immunology; Stomach Neoplasms - metabolism; Studies; Viruses; Zoology; Lahore Pakistan; Pakistan
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1155/2016/8413768

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.