Influenza pandemic with H1N1 (H1N1pdms) causes severe lung damage and “cytokine storm,” leading to higher mortality and global health emergencies in humans and animals. Explaining host antiviral molecular mechanisms in response to H1N1pdms is important for the development of novel therapies. In this study, we organised and analysed multimicroarray data for mouse lungs infected with different H1N1pdm and nonpandemic H1N1 strains. We found that H1N1pdms infection resulted in a large proportion of differentially expressed genes (DEGs) in the infected lungs compared with normal lungs, and the number of DEGs increased markedly with the time of infection. In addition, we found that different H1N1pdm strains induced similarly innate immune responses and the identified DEGs during H1N1pdms infection were functionally concentrated in defence response to virus, cytokine-mediated signalling pathway, regulation of innate immune response, and response to interferon. Moreover, comparing with nonpandemic H1N1, we identified ten distinct DEGs (AREG, CXCL13, GATM, GPR171, IFI35, IFI47, IFIT3, ORM1, RETNLA, and UBD), which were enriched in immune response and cell surface receptor signalling pathway as well as interacted with immune response-related dysregulated genes during H1N1pdms. Our discoveries will provide comprehensive insights into host responding to pandemic with influenza H1N1 and find broad-spectrum effective treatment.
{"title":"The Identification Distinct Antiviral Factors Regulated Influenza Pandemic H1N1 Infection","authors":"Baoxin Wang, Hao Zheng, Xia Dong, Wenhua Zhang, Junjing Wu, Hongbo Chen, Jing Zhang, Ao Zhou","doi":"10.1155/2024/6631882","DOIUrl":"https://doi.org/10.1155/2024/6631882","url":null,"abstract":"Influenza pandemic with H1N1 (H1N1pdms) causes severe lung damage and “cytokine storm,” leading to higher mortality and global health emergencies in humans and animals. Explaining host antiviral molecular mechanisms in response to H1N1pdms is important for the development of novel therapies. In this study, we organised and analysed multimicroarray data for mouse lungs infected with different H1N1pdm and nonpandemic H1N1 strains. We found that H1N1pdms infection resulted in a large proportion of differentially expressed genes (DEGs) in the infected lungs compared with normal lungs, and the number of DEGs increased markedly with the time of infection. In addition, we found that different H1N1pdm strains induced similarly innate immune responses and the identified DEGs during H1N1pdms infection were functionally concentrated in defence response to virus, cytokine-mediated signalling pathway, regulation of innate immune response, and response to interferon. Moreover, comparing with nonpandemic H1N1, we identified ten distinct DEGs (AREG, CXCL13, GATM, GPR171, IFI35, IFI47, IFIT3, ORM1, RETNLA, and UBD), which were enriched in immune response and cell surface receptor signalling pathway as well as interacted with immune response-related dysregulated genes during H1N1pdms. Our discoveries will provide comprehensive insights into host responding to pandemic with influenza H1N1 and find broad-spectrum effective treatment.","PeriodicalId":507859,"journal":{"name":"International Journal of Microbiology","volume":"24 12","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139443693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Techilo Habtemariam Mengesha, M. Ali, Mulugeta Mengistu, Demissie Assegu Fenta
Background. Vancomycin-resistant Enterococci (VRE) is a global health problem and responsible for healthcare-associated infections (HAIs) in patients with prolonged hospital stay, severe underlying disease, and previous broad-spectrum antibiotic therapy. These bacteria can cross-resist and transfer drug-resistant genes to other potentially pathogenic bacteria. Therefore; this study was aimed to determine the gastrointestinal colonization rate of VRE, its antimicrobial susceptibility profile, and associated factors among hospitalized patients. Methods. Prospective cross-sectional study was conducted using stool samples from 223 patients admitted to different wards at Hawassa University Comprehensive Specialized Hospital, from April 1 to June 30, 2021. Patients admitted to the hospital for more than 48 hours for various medical conditions were included. Sociodemographic and clinical characteristics were collected using a structured questionnaire. Fecal specimens were cultured on Enterococci selective media. Enterococcus species were identified using their growth and mannitol fermentation properties. Vancomycin resistance was screened using both the Kirby–Bauer disk diffusion method and a vancomycin E-test strip. Data were entered and analyzed using SPSS version 25. Descriptive and logistic regressions were used to determine the frequency and association of factors with the VRE colonization rate. A p value of <0.05 was considered statistically significant. Results. A total of 223 fecal specimens were collected and processed, and 141 (63.2%) them were positive for Enterococci. The predominant species was E. faecalis 65 (46.1%) followed by E. faecium 76 (53.9%). In this study, the gastrointestinal colonization rate of VRE was 15 (6.7%) and all the species belong to E. faecium. Study participants who had no formal education (AOR = 4.26, 95% CI: 1.01, 18.06), hospitalized patients for >2 weeks (AOR = 4.10, 95% CI: 1.08, 15.57), and those who had a history of treatment with vancomycin (AOR = 4.77, 95% CI: 1.26, 18.09) were more likely to be colonized with vancomycin-resistant Enterococci. More than 95% of Enterococci isolates were susceptible to linezolid, whereas 70.2%, 63.1%, 56.7%, and 53.9% were resistant to tetracycline, erythromycin, penicillin, and ampicillin, respectively. Among the total Enterococci isolated, 141 (54.6%) were multidrug resistant. Conclusions. In our study, high proportion of vancomycin-resistant Enterococci was found. Previous exposure to antibiotics and hospital stay were significant factors for VRE gut colonization. The isolated Enterococci showed variable degrees of resistance to commonly prescribed antibiotics which leads to a worldwide problem multidrug resistance. Therefore, periodic surveillance on antimicrobial resistance pattern, adhering to rational use of antibiotics, and implementing infection prevention protocols may reduce colonization by VRE.
{"title":"High Gastrointestinal Colonization Rate of Vancomycin-Resistant Enterococci among Hospitalized Patients: Potential Source for Resistant Gene","authors":"Techilo Habtemariam Mengesha, M. Ali, Mulugeta Mengistu, Demissie Assegu Fenta","doi":"10.1155/2024/6430026","DOIUrl":"https://doi.org/10.1155/2024/6430026","url":null,"abstract":"Background. Vancomycin-resistant Enterococci (VRE) is a global health problem and responsible for healthcare-associated infections (HAIs) in patients with prolonged hospital stay, severe underlying disease, and previous broad-spectrum antibiotic therapy. These bacteria can cross-resist and transfer drug-resistant genes to other potentially pathogenic bacteria. Therefore; this study was aimed to determine the gastrointestinal colonization rate of VRE, its antimicrobial susceptibility profile, and associated factors among hospitalized patients. Methods. Prospective cross-sectional study was conducted using stool samples from 223 patients admitted to different wards at Hawassa University Comprehensive Specialized Hospital, from April 1 to June 30, 2021. Patients admitted to the hospital for more than 48 hours for various medical conditions were included. Sociodemographic and clinical characteristics were collected using a structured questionnaire. Fecal specimens were cultured on Enterococci selective media. Enterococcus species were identified using their growth and mannitol fermentation properties. Vancomycin resistance was screened using both the Kirby–Bauer disk diffusion method and a vancomycin E-test strip. Data were entered and analyzed using SPSS version 25. Descriptive and logistic regressions were used to determine the frequency and association of factors with the VRE colonization rate. A p value of <0.05 was considered statistically significant. Results. A total of 223 fecal specimens were collected and processed, and 141 (63.2%) them were positive for Enterococci. The predominant species was E. faecalis 65 (46.1%) followed by E. faecium 76 (53.9%). In this study, the gastrointestinal colonization rate of VRE was 15 (6.7%) and all the species belong to E. faecium. Study participants who had no formal education (AOR = 4.26, 95% CI: 1.01, 18.06), hospitalized patients for >2 weeks (AOR = 4.10, 95% CI: 1.08, 15.57), and those who had a history of treatment with vancomycin (AOR = 4.77, 95% CI: 1.26, 18.09) were more likely to be colonized with vancomycin-resistant Enterococci. More than 95% of Enterococci isolates were susceptible to linezolid, whereas 70.2%, 63.1%, 56.7%, and 53.9% were resistant to tetracycline, erythromycin, penicillin, and ampicillin, respectively. Among the total Enterococci isolated, 141 (54.6%) were multidrug resistant. Conclusions. In our study, high proportion of vancomycin-resistant Enterococci was found. Previous exposure to antibiotics and hospital stay were significant factors for VRE gut colonization. The isolated Enterococci showed variable degrees of resistance to commonly prescribed antibiotics which leads to a worldwide problem multidrug resistance. Therefore, periodic surveillance on antimicrobial resistance pattern, adhering to rational use of antibiotics, and implementing infection prevention protocols may reduce colonization by VRE.","PeriodicalId":507859,"journal":{"name":"International Journal of Microbiology","volume":"46 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139447671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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