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On the contrary, the rate of development of new antibiotics to treat these emerging superbugs is very slow. Therefore, the aim of this study was to prepare novel nanobiotic formulations to improve the antimicrobial activity of three antibiotics (linezolid, doxycycline, and clindamycin) against Staphylococci. Antibiotics were formulated as nanoemulsions and evaluated for their antimicrobial activities and cytotoxicities. Cytotoxicity of the conventional antibiotics and nanobiotics was analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay on rat hepatocytes. Half-maximal inhibitory concentration (IC50) was estimated from an experimentally derived dose-response curve for each concentration using GraphPad Prism software. Upon quantitative assessment of Staphylococcus biofilm formation, eighty-four isolates (664 %) were biofilm forming.

Linezolid and doxycycline nanobiotics exhibited promising antibacterial activities. On the contrary, clindamycin nanobiotic exhibited poor antibacterial activity. Minimum biofilm inhibitory concentrations showed that 738 %, 45%, and 5% of respectively. Results of this study revealed that antibiotics loaded in nanosystems had a higher antimicrobial activity and lower cytotoxicities as compared to those of conventional free antibiotics, indicating their potential Nicotinic Acid Catabolism Modulates Bacterial Mycophagy in Burkholderia gladioli Burkholderia gladioli strain NGJ1 exhibits mycophagous activity on a broad range demonstrate that the nicotinic acid (NA) catabolic pathway in NGJ1 is required for mycophagy. NGJ1 is auxotrophic to NA and it potentially senses R. solani as a NA source. Mutation in the nicC and nicX genes involved in NA catabolism renders defects in mycophagy and the mutant bacteria are unable to utilize R.

solani extract as the sole nutrient source. As supplementation of NA, but not FA ability of ΔnicC/ΔnicX mutants, we anticipate that NA is not required as a transcriptional regulator that functions as a negative regulator of the NA catabolic pathway is upregulated in ΔnicC/ΔnicX mutant and upon NA supplementation the nicR expression is reduced to the basal level in both the mutants. The ΔnicR mutant produces excessive biofilm and is completely defective in swimming motility. On the other hand, ΔnicC/ΔnicX mutants are compromised in swimming motility as well as biofilm formation, potentially due to the upregulation of nicR. Our data suggest that a defect in NA catabolism alters the NA pool in the bacterium and upregulates nicR which in turn suppresses bacterial motility as well as biofilm formation, leading to mycophagy defects. IMPORTANCE Mycophagy is an important trait through which certain bacteria forage over fungal mycelia and utilize fungal biomass as a nutrient source to thrive in hostile environments. The present study emphasizes that nicotinic acid (NA) is important for bacterial motility and biofilm formation during mycophagy by Burkholderia gladioli strain NGJ1.

Defects in NA catabolism potentially alter the cellular NA pool, upregulate the expression of nicR, a negative regulator of biofilm, and therefore suppress bacterial motility as well as biofilm formation, Conflict of interest statement: The authors declare no conflict of interest. Antibiofilm potential of 16-oxo-cleroda-3, 13(14) E-diene-15 oic acid and its five new γ-amino γ-lactone derivatives against methicillin resistant Staphylococcus aureus and Streptococcus mutans. Center for Chemical and Biological Sciences, University of Karachi, Karachi Center for Chemical and Biological Sciences, University of Karachi, Karachi Center for Chemical and Biological Sciences, University of Karachi, Karachi 75270, Pakistan; Hamdard Al-Majeed College of Eastern Medicine, Hamdard The clerodane diterpenoids 16-oxo-cleroda-3, 13(14) E-diene-15 oic acid (1) and kolavenic acid (2) isolated from Polyalthia longifolia var. pendula (Linn.) were previously reported for their antimicrobial activity. Thus Colanic acid polymer was designed to investigate the biofilm inhibiting potential of these diterpenoids Staphylococcus aureus (MRSA), Streptococcus mutans, Klebsiella pneumoniae and Proteus mirabilis. Compounds 1 and 3 at 10-20 μg/mL were found to be bacteriostatic and significantly reduced the biofilm formation and metabolically active cells of MRSA and S.

 mutans up to 90%. Parental diterpenoid (1) at 10 and 16 μg/mL significantly eradicated the preformed biofilm of both pathogens. Both the compounds also delayed acid production at minimum inhibitory (MIC) and sub-inhibitory concentrations (sub MIC). Florescence and scanning electron microscopy further confirms the biofilm inhibiting potential of compounds 1 and 3 and displayed disrupted biofilms at MIC and sub MIC levels. Colanic acid of MRSA and S.