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Pseudomonas aeruginosa strain SW1 is an aerobic, motile, Gram-negative, and rod-shaped bacterium isolated from degraded seaweeds. Based on the 16S rDNA sequence and MALDI TOF analysis, the strain SW1 exhibits 100% similarity with P. aeruginosa DSM 50071, its closest phylogenetic neighbour. P. aeruginosa is an opportunistic pathogen that can infect plants, animals and humans. The complete genome of P. aeruginosa strain SW1 consists of a single circular chromosome with 23,258,857 bp (G+C content of 66%), including 6734 coding DNA sequences, 8 rRNA, and 63 tRNA sequences. The genome of the P. aeruginosa SW1 contains genes for biosynthesis of alginate (AlgA.

Human diseases are generally influenced by SNPs (single nucleotide polymorphisms). The mutations in amino acid residues generated by deleterious SNPs contribute to the structural and functional diversity of the encoded protein. Tumor necrosis factor-α (TNF-α), Glucocorticoid receptor gene (NR3C1), and Cytochrome P450 3A5 (CYP3A5) play a key role in glucocorticoid resistance susceptibility in humans. Possible causative mutations could be used as therapeutic targets and diagnostic markers for glucocorticoid resistance. This study evaluated the missense SNPs of TNF-α, NR3C1, and CYP3A5 to predict their impact on amino acid changes, protein interaction, and functional stability. The protein sequence of dbSNP was obtained and used online in silico method to screen deleterious mutants for the in silico analysis. In the coding regions of TNF-α, NR3C1, and CYP3A5, 14 deleterious mutations were discovered. The protein functional and stability changes in the amino acid between native and mutant energy were identified by analyzing the changes in the hydrogen bonding of these mutants from native, which were all measured using Swiss PDB and PyMOL. F446S and R439K had the highest root-mean-square deviation (RMSD) values among the 14 deleterious mutants. Additionally, the conserved region of amino acid protein interaction was analyzed. This study could aid in the discovery of new detrimental mutations in TNF-α, NR3C1, and CYP3A5, as well as the development of long-term therapy for corticosteroid resistance in several inflammatory diseases. However, more research into the deleterious mutations of the TNF-α, NR3C1, and CYP3A5 genes is needed to determine their role in corticosteroid resistance.

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