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Protein Subunit Vaccines and Recombinant DNA Technology
Published in F. Y. Liew, Vaccination Strategies of Tropical Diseases, 2017
There are numerous reports in the literature on the problem of plasmid stability.31 Increases in the expression of recombinant genes generally leads to a reduction in growth rate and may result in morphological changes such as filamentation and increased cell fragility. A mutant which has either lost the plasmid or has undergone structural rearrangements such that the recombinant gene expression is lost or the copy number is reduced will confer upon that cell a faster growth rate and may quickly take over the culture.
Imipenem–Cilastatin and Imipenem–Relebactam
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Yoshiro Hayashi, David L. Paterson
Imipenem, like all other beta-lactam agents, inhibits bacterial cell wall synthesis by binding to and inactivating relevant transpeptidases, known as PBPs (Rodloff et al., 2006). Imipenem binds preferentially to PBP2 and PBP1, the transpeptidases implicated in elongation of the bacterial cell wall, and has weak affinity for PBP3, the primary target of aminopenicillins and cephalosporins. Meropenem, doripenem, and ertapenem have relatively higher affinity to PBP3 than imipenem (Zhanel et al., 2007). Binding to PBP2 produces the lemon shapes that occur when E. coli is exposed to imipenem, in contrast to the long filaments that result from exposure to penicillins and cephalosporins, which seem to be consequent on the binding of those drugs to PB 3 (Spratt et al., 1977; Majcherczyk and Livermore, 1990). When P. aeruginosa cultures were exposed to either ceftazidime (which induces filamentation) or to imipenem, ceftazidime, treatment resulted in much more release of a lipopolysaccharide endotoxin than similar treatment with imipenem (Jackson and Kropp, 1992). The significance of this finding in clinical practice has not been established, however.
Clinical Implications of Interkingdom Fungal and Bacterial Biofilms
Published in Chaminda Jayampath Seneviratne, Microbial Biofilms, 2017
Gordon Ramage, Lindsay E. O’Donnell, Ryan Kean, Eleanor Townsend, Ranjith Rajendran
P. aeruginosa has also been shown to inhibit A. fumigatus filamentation via the release of molecules involved in intracellular communication [228]. Investigations into the interactions between these two are limited; however, the release of small molecules designed to inhibit fungal growth appear to be the primary form of interaction. One particular group of metabolites known as phenazines have been reported to inhibit A. fumigatus biofilm formation; however, it was also found that A. fumigatus was able to convert these metabolites released by P. aeruginosa to produce fungal siderophores, which may in turn influence CF progression [234]. Furthermore, P. aeruginosa releases the metalloprotease elastase, which has been shown to be toxic to host cells [9]. It was found that elastase production was constitutive, but became significantly increased in the presence of A. fumigatus during biofilm coculture. Furthermore, elastase was cytotoxic to human lung cells, therefore indicating that the presence of both of these pathogens could synergistically contribute towards enhanced pathogenicity [9]. Thus, in general, evidence suggests that the co-isolation of both of these organisms indicates a poorer prognosis; however, the relationship between the two remains poorly understood and requires further investigation into their polymicrobial interactions.
Drug design strategies for the treatment azole-resistant candidiasis
Published in Expert Opinion on Drug Discovery, 2022
Setareh Moghimi, Mohammad Shafiei, Alireza Foroumadi
Biofilm formation is the main virulence factor contributing to C. albican’s pathogenesis. Upon hyphal filamentation caused by Candida cells, the infected surface area is increased to reach nutrients. By developing an exopolymeric matrix layer known as mature biofilm, a physical barrier is built between cells and the drug/immune system [22]. The biofilm formation allows yeast cells to adhere to biological or inert surfaces like medical implant devices and causes serious conditions like catheter-related infections. The majority of the extracellular matrix’s components are identical to those found in fungal cell walls, including glucan polymers. Further, the efflux pumps are expressed to flush out the entrapped drugs in biofilm layers. Consequently, C. albicans cells with biofilms display extreme resistance to azoles or any conventional antifungal therapy, which indicates the unmet need for new antibiofilm and antifungal agent discovery.
Proteomic interrogation of antibiotic resistance and persistence in Escherichia coli – progress and potential for medical research
Published in Expert Review of Proteomics, 2020
Danfeng Zhang, Yuanqing Hu, Qiuqiang Zhu, Jiafu Huang, Yiyun Chen
The first reported method for isolating persisters involved lysis of susceptible E.coli HM22 cells by 100 µg/mL of ampicillin following treatment with 50µg/mL of chloramphenicol to induce persister formation (Table 1). Upon ampicillin treatment, only intact persister cells were collected by sedimentation [17]. This method is easily performed, but debris of susceptible cells is often still present in the sediment due to poor separation efficiency during sedimentation, leading to proteins of susceptible cells and persisters being analyzed by proteomic technologies together, instead of analysis of persister proteins alone. To minimize the amount of cell debris, the antibiotic cephalexin was used in a highly effective persister enrichment method which induced extensive filamentation of susceptible cells only [120]. Only 1 h treatment was sufficient to allow for the isolation of persister cells from the culture by filtration, thus decreasing the antibiotic exposure time and reducing persister sample contamination with debris from dead cells in the sample when compared to the ampicillin-lysis method. Cephalexin, a β-lactam antibiotic, targets penicillin-binding protein (PBP) 3, which is essential for peptidoglycan synthesis in the process of cell division. Furthermore, it does not induce lysis at once, but first induces severe filamentation of susceptible cells filament prior to lysis. In this way, cephalexin only acts on susceptible cells and does not affect drug tolerant persisters, enabling the enrichment of persister isolation via filtration.
Susceptibility to biofilm formation on 3D-printed titanium fixation plates used in the mandible: a preliminary study
Published in Journal of Oral Microbiology, 2020
Lukasz Palka, Justyna Mazurek-Popczyk, Katarzyna Arkusz, Katarzyna Baldy-Chudzik
The results of the microbiological tests were confirmed by visualization of bacterial cells using SEM microscopy. The analysis showed both the surface shape of the 3D-printed plates and the specific manner of growth for each of the tested species after 48 hours of culture. S. mutans formed dense biofilms covering most of the titanium plate surface (Figure 3). S. epidermidis also created conglomerates on the plate surface, mostly covering the depressions (Figure 4). Smaller conglomerates and sparse cells were revealed in the biofilm of S. aureus (Figure 5). SEM images show L. rhamnosus cells forming a characteristic biofilm network. Newly formed cells lengthened the network by locating in the wells/depressions of the plate (Figure 6). Extensive and highly structured biofilm with the filamentation was observed in the case of C. albicans growth (Figure 7).