It also induced IL-1β, IL-18, TNF-α, and up-regulated NLRP3, ro-IL-1β, Caspase-1, Pro-Caspase-1, and GSDMD-N in culture. Similar to the NLRP3 inhibitor INF39, MXSG (0.1, 0.2, and 0.4 mg/mL) suppressed pyroptosis induced by infection and decreased IL-1β ( < 0.001), IL-18, TNF-α in culture. MXSG down-regulated NLRP3, pro-IL-1β, Caspase-1, pro-Caspase-1, and GSDMD-N in infected cultures and mitigated NLRP3 overexpression-induced pyroptosis. MXSG mitigates -induced pyroptosis in A549 cells via the NLRP3 inflammasome. MXSG mitigates M. pneumoniae-induced pyroptosis in A549 cells via the NLRP3 inflammasome.The 20th century witnessed the dawn of the antibiotic revolution and is now facing the rising phenomenon of antibiotic resistance. In this narrative review, we aim to describe antibiotic resistance in clinical practice settings through population-based studies from different countries reporting the role of misuse of antibiotics in the development of resistance and the clinical and economic burden associated. The misuse of antibiotics was documented in the wide population as well as in hospitals and care facilities. It was mainly reported as over-use and inappropriate prescribing. Improper dosage regimens and longer treatment duration were regarded as pivotal factors related to antibiotic resistance; the emerging strategy of "antibiotic-de-escalation" could be the key to overcome these issues. The investigation of the self-medication attitude revealed widespread antibiotic use without following medical instructions or medical consultation. Moreover, several studies established the association of antibiotic resistance with increased risk of longer hospitalizations and mortality, highlighting the heavy clinical and economic burden of this phenomenon. In this narrative review, the widespread inappropriate use of antibiotics emerged as one of the main causes of antibiotic resistance, which negative outcomes call for the development of antibiotic stewardship programs and global surveillance networks. Emergence and dissemination of colistin-resistant bacteria that harbor mobile colistin resistance ( ) genes pose a dire challenge for the treatment of intractable infections caused by multidrug-resistant bacteria. Current findings on colistin-resistant bacteria in both humans and livestock of the same households highlight the need to identify the dissemination mechanisms of colistin-resistant bacteria. In this study, a comparative genome analysis of colistin-resistant isolates from livestock and humans of the same household was performed to clarify the possible dissemination mechanism of genes among bacteria. Pulsed-field gel electrophoresis and whole-genome sequencing followed by sequence typing of the isolates were performed for assessment of the samples. The study revealed that two colistin-resistant isolates, one each from a pig and a chicken, were phylogenetically similar but not identical to the human isolates obtained from the same household. The comparative genome analysis revealed thaisolates obtained from livestock and residents of the same household. Antibiotics for treating infectious diseases caused by carbapenem-resistant Gram-negative pathogens (CR-GNOs) are very limited in clinical practice. We aim to provide supportive evidence by revealing the combined effect of aztreonam (ATM) and amoxicillin/clavulanic acid (AMC) against GNOs with carbapenem resistance mediated by metallo-β-lactamase (MBL). All isolates were identified by the VITEK system and EDTA inhibitory assays. PCR followed by sequencing was conducted to confirm the genotypes of MBL and extended spectrum β-lactamase (ESBL). Time kill assay was performed to clarify the bactericidal effect of drug combination. A total of 59 MBL-producing CR-GNOs (33 spp. isolates and 26 Pseudomonadales isolates) were identified and there found three MBL genes, namely, , and , with ratios of 76.2%, 11.8% and 11.8%, respectively. The spp. isolates were commonly positive for the ESBL genes, including (18 isolates), (20 isolates) and (8 isolates), while the isolates were in vitro. This study reports a cross-sectional investigation to determine the antimicrobial resistance pattern of the common bacterial contaminants isolated from hospitalized patients in Mogadishu, Somalia. A total of 328 clinical samples comprising urine, blood, vaginal swab, pus aspirates, and stool were collected from a public hospital located in Mogadishu the capital city of Somalia between October 2019 to March 2020. The isolation and biochemical characterization of the bacterial isolates were performed using the conventional culture and biochemical assay tests. Similarly, antimicrobial susceptibility was determined using the Kirby-Bauer disk diffusion. A total of 275 pathogenic bacteria that include , and spp. were detected with an overall detection rate of 78.4% (257/328). Among the bacterial pathogens isolated from clinical specimens, 152 (46.3%) were , 60 (18.3%) were , 10 (3.1%) , 6 (1.8%) , and 1 (0.3%) isolate was found to be sp. The antimicrobial susceptibility assay revealed variablecterial isolates during the management of patients in the hospital. To establish a risk prediction model for carbapenem-resistant Enterobacteriaceae (CRE) bloodstream infection (BSI) in intestinal carriers. CRE screenings were performed every two weeks in hematology department and intensive care unit (ICU). Patients with positive CRE rectal swab screening were identified using electronic medical records from 15 May 2018 to 31 December 2019. Intestinal carriers who developed CRE BSI were compared with those who did not develop CRE infection. A 11 matched case-control study was conducted. The control group was selected by stratified random sampling based on the department to ensure that all the departments were represented. https://www.selleckchem.com/products/mk-0159.html Univariate logistic analysis, multivariate logistic analysis and stepwise regression analysis were carried on a variety of patient factors and microbial factors. A total of 42 cases were included. Multivariate analysis showed that gastrointestinal injury (OR 86.819, 95% CI 2.584-2916.592, =0.013), tigecycline exposure (OR 14.991, 95% CI 1.816-123.737, =0.