ABSTRACT
Pseudomonas aeruginosa is one of the most common causes of diabetic foot infection globally. This study aimed to determine the global distribution of P. aeruginosa isolated from diabetic foot ulcer infection. PRISMA procedure was used to perform the current systematic review and meta-analysis. The Web of Science, MEDLINE/PubMed, Scopus, and other databases were searched for studies published in English from 2000 to 2022. Data was analyzed using the Comprehensive Meta-Analysis software (CMA). Keywords and MESH phrases included Pseudomonas aeruginosa, diabetic foot ulcer, P. aeruginosa, and diabetic foot infection. As a result of this review, 16.6% of diabetic foot wound infections were caused by P. aeruginosa. About 37.9% of strains were multidrug resistant (MDR). P. aeruginosa infection rates in diabetic foot ulcers ranged from 0.5 to 100% globally. In total, the prevalence rates of P. aeruginosa in diabetic foot ulcer infection from Asia, Africa, and Western countries were reported at 18.5%, 16.3%, and 11.1%, respectively. Data have shown that the prevalence of P. aeruginosa, particularly MDR strains, isolated from diabetic foot ulcer infection was relatively high; inherent resistance to antibiotics is also high; the wound either does not heal or if it does, it will be delayed. Therefore, timely treatment is essential.
ABSTRACT
Interleukin-33 (IL-33) is a member of the IL-1 family and plays an ambivalent role in autoimmune diseases. IL-33 signals via the ST2 receptor and drives cytokine production in mast cells, basophils, eosinophils, NK cells, and T lymphocyte cells. The vital role of IL-33 as an active component gives rise to aberrant local and systemic damage which has been demonstrated in numerous inflammatory disorders and immune-mediated pathological conditions including multiple sclerosis (MS), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), psoriasis, Sjogren's syndrome, inflammatory bowel disease (IBD), etc. IL-33/ST2 axis can up-regulate pro-inflammatory cytokine release in autoimmune disease, however, in some metabolic diseases like diabetes mellitus type 1 IL-33 can be considered an anti-inflammatory cytokine. The purpose of this review is to discuss selected studies on IL-33/ST2 axis in autoimmune diseases and its potential role as a pathogenic or protective cytokine.
Subject(s)
Autoimmune Diseases , Interleukin-1 Receptor-Like 1 Protein , Interleukin-33 , Autoimmune Diseases/genetics , Autoimmune Diseases/metabolism , Cytokines , Humans , Interleukin-1 Receptor-Like 1 Protein/genetics , Interleukin-1 Receptor-Like 1 Protein/metabolism , Interleukin-33/genetics , Interleukin-33/metabolism , Sjogren's Syndrome/genetics , Sjogren's Syndrome/metabolismABSTRACT
Escherichia coli accounts for nearly 80% of community-acquired and 50% of hospital-acquired urinary tract infections (UTI). This study aimed to evaluate the correlation between biofilm producers and Non-biofilm producers with antibiotic resistance in Uropathogenic Escherichia coli (UPEC) isolated from patients with UTI globally. The search was conducted between 1st 2000 to 30th October 2021 in various databases (PubMed, Scopus, Web of sciences, and Google Scholar) with suitable MeSH terms, and text words. Then, after applying the appropriate inclusion and exclusion criteria on the studies for their selection, the data were analyzed by CMA software. Thirty-seven studies met the eligibility criteria to include. The pooled prevalence of ESBL and MDR isolates were reported 37.9%, and 65.8%, respectively. Biofilm formation varied between 13.3% and 99% all over the world. A total of 74.4% of all isolates were biofilm producers, out of which 28.6%, 35.2%, and 38.6% showed strong, moderate, and weak bioï¬lm. The highest and lowest resistance was against Amoxicillin and Meropenem with the prevalence of 80.8%, and 13%, respectively. Fourteen out of 17(82.35%) studies reported a positive correlation between biofilm and antibiotic resistance. Findings showed high numbers of isolates were able to form biofilm, which is one of the factors of antibiotic resistance, and this has been confirmed by the positive significant correlation between biofilm formation and antibiotic resistance that has been reported by studies included. Therefore, due to the importance of biofilm in the etiology of UTI caused by UPEC, it should be prevented; consequently, bacterial resistance can be reduced and controlled.
