Bioassay directed identification of royal jelly’s active compounds against the growth of bacteria capable of infecting cutaneous wounds

Antibiotic-resistant bacteria continue to be of major health concern world-wide. Thus, it is of great interest to study the biological properties and determine active compounds in natural products likely to be used as new health remedies. Therefore, the main objective of this work is to test the antibacterial activity of royal jelly samples, defatted royal jelly samples and their ethyl ether extracts against bacteria capable of infecting cutaneous wounds in humans and animals, and to recognize major bioactive compounds by using bioassay directed identification. The microorganisms used in the study were Staphylococcus aureus (including Methicillin-resistant and sensitive strains), Staphylococcus epidermidis, Micrococcus luteus, Streptococcus uberis, Enterococcus faecalis, Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae. The activity of royal jelly samples to inhibit bacterial growth was assessed by using well-difussion tests. Direct bioautography was used to identify bioactivity, and uv-visible spectroscopy and gas chromatography-mass spectrometry were used to identify bioactive compounds. Overall, royal jelly samples showed higher growth inhibition activity against Gram positive bacteria as compared to Gram negative bacteria. The growth of bacterial strains belonging to the Enterococcus and Streptococcus genders was less affected by the presence of royal jelly than bacterial strains of the Staphylococcus gender did. Compounds with antibacterial activity were found in the ethyl ether extract of royal jelly samples. 10-hydroxy-2-decenoic acid was the major component identified in the purified fraction obtained by bioassay guided fractionation of the ethyl ether extract. In conclusion, bioactivity of royal jelly samples is mainly due to their 10-hydroxy-2-decenoic acid content.Fil: Garcia, Mariana Celeste. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas, Fisicoquímicas y Naturales. Departamento de Microbiología e Inmunología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Finola, Mónica S.. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas, Fisicoquímicas y Naturales. Departamento de Microbiología e Inmunología; ArgentinaFil: Marioli, Juan Miguel. Universidad Nacional de Río Cuarto. Facultad de Ciencias Exactas Fisicoquímicas y Naturales. Departamento de Química; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

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TREM-1 expression on neutrophils and monocytes of septic patients: relation to the underlying infection and the implicated pathogen

<p>Abstract</p> <p>Background</p> <p>Current knowledge on the exact ligand causing expression of TREM-1 on neutrophils and monocytes is limited. The present study aimed at the role of underlying infection and of the causative pathogen in the expression of TREM-1 in sepsis.</p> <p>Methods</p> <p>Peripheral venous blood was sampled from 125 patients with sepsis and 88 with severe sepsis/septic shock. The causative pathogen was isolated in 91 patients. Patients were suffering from acute pyelonephritis, community-acquired pneumonia (CAP), intra-abdominal infections (IAIs), primary bacteremia and ventilator-associated pneumonia or hospital-acquired pneumonia (VAP/HAP). Blood monocytes and neutrophils were isolated. Flow cytometry was used to estimate the TREM-1 expression from septic patients.</p> <p>Results</p> <p>Within patients bearing intrabdominal infections, expression of TREM-1 was significantly lower on neutrophils and on monocytes at severe sepsis/shock than at sepsis. That was also the case for severe sepsis/shock developed in the field of VAP/HAP. Among patients who suffered infections by Gram-negative community-acquired pathogens or among patients who suffered polymicrobial infections, expression of TREM-1 on monocytes was significantly lower at the stage of severe sepsis/shock than at the stage of sepsis.</p> <p>Conclusions</p> <p>Decrease of the expression of TREM-1 on the membrane of monocytes and neutrophils upon transition from sepsis to severe sepsis/septic shock depends on the underlying type of infection and the causative pathogen.</p