Acinetobacter baumannii is a Gram-negative coccobacillus responsible for severe hospital-acquired infections, particularly in intensive care units (ICUs). The current study was designed to characterize the virulence traits of biofilm-forming carbapenem-resistant A. baumannii causing pneumonia in ICU patients using a Galleria mellonella model. Two hundred and thirty patients with hospital-acquired or ventilator-associated pneumonia were included in our study. Among the total isolates, A. baumannii was the most frequently isolated etiological agent in ICU patients with pneumonia (54/165, 32.7%). All A. baumannii isolates were subjected to antimicrobial susceptibility testing by the Kirby–Bauer disk diffusion method, while the minimum inhibitory concentrations of imipenem and colistin were estimated using the broth microdilution technique. The biofilm formation activity of the isolates was tested using the microtiter plate technique. Biofilm quantification showed that 61.1% (33/54) of the isolates were strong biofilm producers, while 27.7% (15/54) and 11.1% (6/54) showed moderate or weak biofilm production. By studying the prevalence of carbapenemases-encoding genes among isolates, bla_OXA-23-_like was positive in 88.9% of the isolates (48/54). The Bla_NDM gene was found in 27.7% of the isolates (15/54 isolates). Bla_OXA-23-_like and bla_NDM genes coexisted in 25.9% (14/54 isolates). Bap and bla_PER-1 genes, the biofilm-associated genes, coexisted in 5.6% (3/54) of the isolates. For in vivo assessment of A. baumannii pathogenicity, a Galleria mellonella survival assay was used. G. mellonella survival was statistically different between moderate and poor biofilm producers (p < 0.0001). The killing effect of the strong biofilm-producing group was significantly higher than that of the moderate and poor biofilm producers (p < 0.0001 for each comparison). These findings highlight the role of biofilm formation as a powerful virulence factor for carbapenem-resistant A. baumannii that causes pneumonia in the ICU.

Probiotics can potentially prevent and treat diseases. We examined the inhibitory activity of bacteriocin-like inhibitory substances (BLISs) from potentially probiotic lactobacilli and streptococci on Candida albicans and non-Candida albicans clinical isolates from women with vulvovaginitis. Using agar well diffusion assays, BLISs inhibited both Candida albicans and non-Candida albicans isolates. The BLIS from L. pentosus isolates had the highest anti-Candida activity (33/45; 73.3%), followed by BLISs from isolates of L. paracasei subsp. paracasei (31/45; 68.9%), L. rhamnosus I (30/45; 66.7%), L. delbrueckii subsp. lactis I (30/45; 66.7%), and S. uberis II (30/45; 66.7%). Upon characterization according to the retained activity under variable physical and chemical conditions, the BLISs showed stability against heat, pH, and surfactants, but were protease-sensitive, which suggests a proteinaceous nature of the active substances. Using crystal violet assays, the BLISs reduced the Candida biofilm biomass significantly as compared to a control group that lacked BLISs. In vivo testing of the antagonistic activity was performed using the Galleria mellonella (G. mellonella) larvae model. BLISs significantly improved survival in G. mellonella larvae treated with Candida isolates on the first, second, and seventh days, as compared to larvae inoculated with Candida only (p < 0.01). The results show that BLISs can be used as biotherapeutic agents in vulvovaginal candidiasis.

The increasing incidence of carbapenem-resistant Klebsiella pneumoniae (CRKP) strains is considered as a terrifying public health concern. This study target was to gain a further insight into the virulence traits of CRKP isolates in Egypt. The study was carried out by using 43 clinical K. pneumoniae isolates. Antibiotic susceptibility testing, biofilm formation assay, and molecular characterization of carbapenemase and virulence genes were done for all isolates. In addition, the genotypic relationship between CRKP isolates was identified by using enterobacterial repetitive intergenic consensus-polymerase chain reactions (ERIC-PCRs). A Galleria mellonella survival assay was adopted for in vivo testing of virulence of the CRKP. Carbapenem resistance was exhibited among 58% (25/43) isolates. Minimum inhibitory concentration values of carbapenem-resistant K. pneumoniae (CRKP) ranged from 32 to 128 μg/mL. Biofilm assay has revealed that 21 isolates (49%) had moderate biofilm formation and 11 isolates (25.5%) were strong biofilm producers. Bla _NDM-1 was recognized in 20.9% (9 / 43) of the isolates, while bla _OXA-48 was observed in 18.5% (8/43). Type 3 fimbriae ( mrkD ) and entB were addressed among 72.1% and 62.8% of K. pneumoniae isolates, respectively. The ybtS and iutA genes were detected among 44.2% and 37.2% of the isolates, respectively. ERIC-PCR showed 23 genetic profiles among CRKP isolates. CRKP biofilm producers were virulent according to the G. mellonella model, which indicates the importance of biofilm as a virulence trait among CRKP. This study indicates the emergence of CRKP with increased virulence traits, especially biofilm formation, in Egypt. This alarming report highlights the ongoing need for effective screening procedures and strict infection control measures.

Behçet's disease (BD) is a chronic inflammatory disease. Immunological defects have been shown to play a significant role in the progression of BD. The serum levels of two long non-coding RNAs (lncRNAs), NEAT1 and MALAT1, were examined in patients with BD to identify their role in the disease pathogenesis. Both lncRNAs were mentioned as essential regulators of innate immune responses and have a crucial role in inflammatory diseases. Fifty patients with BD and a similar number of control individuals were involved in our study. At enrollment, data was collected from patients and controls, and the disease severity in active cases was determined using the Behçet's Disease Current Activity Form (BDCAF). Levels of the two studied biomarkers in the serum, NEAT1 and MALAT1, were investigated by quantitative RT-PCR (qRT-PCR). NEAT1 levels were significantly turned down in BD patients (fold changes = 0.77, p = 0.0001) and correlated negatively with the BDCAF (r = −0.41; p = 0.003). On the other hand, the MALAT1 levels were significantly up-regulated in BD patients (fold changes = 2.65, p = 0.003). Serum levels of NEAT1 were significantly decreased in patients with active states than in stationary cases (0.387 versus 1.99, respectively; p = 0.01) and compared with controls (p = 0.001). Also, NEAT1 levels were significantly increased in patients with stationary states compared to controls (p = 0.03). There was a positive association between NEAT1 and MALAT1 levels among BD patients (r = 0.29, p = 0.04). Our findings demonstrate a possible role of NEAT1 and MALAT1 in the pathogenesis of BD.

Introduction: Multiple sclerosis (MS) is an immune-mediated disorder. Long noncoding RNAs (lncRNAs, LncR, Linc RNA) have role in many autoimmune and inflammatory disorders, including MS. LincR-Gng2-5 AS locus in T helper 1 cell (TH1) and LincR-Epas1-3AS in T helper 2 cell (TH2) cell were located in a genomic region rich in genes code for proteins with immune regulatory function. Our aim was to evaluate the LincR-Gng2-5′ and LincR-Epas1-3′AS fold change in blood of MS patients versus healthy controls and correlate it with disease severity, assessed based on Expanded Disability Status Scale (EDSS). Material and Methods: Sixty MS patients 42 relapsing remitting (RR, RRMS), 18 Secondary progressive (SP, SPMS) and sixty controls (age-matched and sex-matched) were studied. Blood of patients and control group undergone the investigation of LincR-Gng2-5′ and LincR-Epas1-3′AS fold change by real-time PCR. Fold change >2 and p < .05 represent significant result. Results: LincR-Gng2-5′ was significantly upregulated in MS patients with mean fold change (2.559) and (p = .03). Meanwhile, LincR-Epas1-3′AS levels were significantly downregulated with mean fold change (0.5964) and (p < .004). Patients with SP showed a significantly higher level of LincR-Gng2-5-fold change (3.71 ± 0.7) than that of RR (1.33 ± 0.3). LincR-Epas1-3′AS was markedly reduced among SP (0.43 ± 0.2) than that of RR (0.66 ± 0.1) but with no significant difference. As regards disease severity (EDSS); there was a significant positive correlation with LincR-Gng2-5 and negative correlation with LincR-Epas1-3′AS. LincR- Gng2-5and LincR-Epas1-3′AS, both are dysregulated in MS patient suggesting a role in disease pathogenesis. Conclusion: LincR-Gng2-5 AS and LincR-Epas1-3′AS fold change are correlated to MS severity (EDSS).

Background: Globally, hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death due to a lack of early predictive and/or diagnostic tools. Thus, research for a new biomarker is important. LncRNAs play a functional role in target gene regulation and their deregulation is associated with several pathological conditions including HCC. Objective: This study aimed to explore the diagnostic potential of two LncRNAs MALAT1 and CASC2 in HCC compared to the routinely used diagnostic biomarker. Materials and methods: The current study is a case-control study carried out at Fayoum University Hospital and conducted on 89 individuals. The study included three groups of 36 HCC patients on top of HCV(HCC/HCV), 33 HCV patients, and 20 healthy volunteers as a control group. All study subjects were subjected to radiological examinations. The determination of CBC was performed by the automated counter and liver function tests by the enzymatic method were performed. In addition, HCV RNA quantification and the expression level of two LncRNAs (MALAT1 and CASC2) were performed by qRT-PCR. Results: The results revealed a statistically significant difference between study groups regarding liver function tests with a higher mean in HCC/HCV group. Also, serum MALAT1 significantly up-regulated in HCV (11.2±2.8) and HCC/HCV (4.56±1.4) compared to the control group. Besides, serum CASC2 levels in the HCV group were significantly upregulated (14.9±3.6), while, downregulated in the HCC group (0.16± 0.03). Furthermore, The ROC analysis for diagnostic efficacy parameters indicated that CASC2 has higher accuracy (94.6%) and sensitivity (97.2%) for HCC diagnosis than AFP with an accuracy of (90.9%), sensitivity (69.4%), and MALAT1 showed an accuracy of (56.9%), sensitivity (72.2%). Conclusion: Our study results indicated that CASC2 is a promising biomarker and is considered better and could help in HCC diagnosis on top of HCV than MALAT1 and the routine biomarker AFP.