Staphylococcus aureus is a major hospital and community pathogen having the aptitude to cause a wide variety of infections in men. The ability of microorganisms to produce biofilm facilitates them to withstand the host immune response and is recognized as one factor contributing to chronic or persistent infections. It was demonstrated that the ica-encoded genes lead to the biosynthesis of polysaccharide intercellular adhesion (PIA) molecules, and may be involved in the accumulation phase of biofilm formation. Different studies have shown the decisive role of the ica gene as virulence factors in staphylococcal infections. This study was carried out to demonstrate the relationship between ica gene and production of slime layer in S. aureus strains. Sixty S. aureus strains were isolated from patients. The isolates were identified morphologically and biochemically following standard laboratory methods. After identification, the staphylococcal isolates were maintained in trypticase soy broth (TSB), to which 15% glycerol was added, and stored at -20°C. Slime formation and biofilm assay was monitored. A PCR assay was developed to identify the presence of icaD (intercellular adhesion gene) gene in all isolates. Thirty-nine slime producing colonies with CRA plates (65%) formed black colors, the remaining 21 isolates were pink (35%). In the quantitative biofilm assay 35 (58%) produced biofilm while 25 (42%) isolates did not exhibit this property. All isolates were positive for detection of icaD gene by PCR method. The interaction of icaA and icaD in the investigated isolates may be important in slime layer formation and biofilm phenomena. We propose PCR detection of the ica gene locus as a rapid and effective method to be used for discrimination between potentially virulent and nonvirulent isolates, with implications for therapeutic and preventive measures pertainin to the management of colonized indwelling catheters.

Interleukin (IL)-33, a member of IL-1 cytokine family, is produced by various immune cells and acts as an alarm to alert the immune system after epithelial or endothelial cell damage during cell necrosis, infection, stress, and trauma. The biological functions of IL-33 largely depend on its ligation to the corresponding receptor, suppression of tumorigenicity 2 (ST2). The pathogenic roles of this cytokine have been implicated in several disorders, including allergic disease, cardiovascular disease, autoimmune disease, infectious disease, and cancers. However, alerted levels of IL-33 may result in either disease amelioration or progression. Genetic variations of IL33 gene may confer protective or susceptibility risk in the onset of autoimmune diseases. The purpose of this review is to discuss the involvement of IL-33 and ST2 in the pathogenesis of a variety of autoimmune disorders, such as autoimmune rheumatic, neurodegenerative, and endocrine diseases.