epidermal-growth-factor and Staphylococcal-Infections

Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative processes in the lung. ADAM10 and ADAM17 are the most prominent members of this protease family. They are constitutively expressed in most lung cells and, as recent research has shown, are the pivotal shedding enzymes mediating acute lung inflammation in a cell-specific manner. ADAM17 promotes endothelial and epithelial permeability, transendothelial leukocyte migration, and inflammatory mediator production by smooth muscle and epithelial cells. ADAM10 is critical for leukocyte migration and alveolar leukocyte recruitment. ADAM10 also promotes allergic asthma by driving B cell responses. Additionally, ADAM10 acts as a receptor for Staphylococcus aureus (S. aureus) α-toxin and is crucial for bacterial virulence. ADAM8, ADAM9, ADAM15, and ADAM33 are upregulated during acute or chronic lung inflammation, and recent functional or genetic analyses have linked them to disease development. Pharmacological inhibitors that allow us to locally or systemically target and differentiate ADAM-family members in the lung suppress acute and asthmatic inflammatory responses and S. aureus virulence. These promising results encourage further research to develop therapeutic strategies based on selected ADAMs. These studies need also to address the role of the ADAMs in repair and regeneration in the lung to identify further therapeutic opportunities and possible side effects.

Topics: ADAM Proteins; Animals; Asthma; B-Lymphocytes; Bacterial Toxins; Epidermal Growth Factor; Gene Expression Regulation, Enzymologic; Hemolysin Proteins; Humans; Pneumonia, Staphylococcal; Proteolysis; Staphylococcal Infections; Staphylococcus aureus; Transendothelial and Transepithelial Migration; Tumor Necrosis Factor-alpha; Virulence Factors

The objective was to evaluate Staphylococcus aureus and Pseudomonas aeruginosa colonisation of wounds treated with recombinant epidermal growth factor (EGF) and platelet-rich plasma (PRP); to analyse the susceptibility profiles of S. aureus and P. aeruginosa isolates from wounds treated with EGF and PRP; and to describe the presence of infection in EGF-treated and PRP-treated wounds. Experimental study was performed using clinical specimens collected with swabs. Patients were treated with PRP and EGF in the outpatient clinic of a university hospital. Forty-three isolates were obtained from 31 patients, 41.9% (13/31) of whom had been treated with EGF and 58.0% (18/31) with PRP. Ten of the 43 isolates were identified as S. aureus, 60.0% (6/10) of which were isolated from PRP-treated wounds. Among the 33 P. aeruginosa isolates, 66.6% (22/33) were isolated from PRP-treated wounds. Regarding antimicrobial susceptibility, only one strain isolated from an EGF-treated wound was identified as methicillin-resistant S. aureus (MRSA). Among the P. aeruginosa isolates, one obtained from a patient treated with EGF was multidrug-resistant. Patients treated with EGF had no infections during the follow-up period, and there was a significant difference between the 1st and 12th week in wound infection improvement in patients treated with PRP (P = .0078).

Topics: Drug Resistance, Bacterial; Epidermal Growth Factor; Gels; Humans; Platelet-Rich Plasma; Pseudomonas aeruginosa; Pseudomonas Infections; Recombinant Proteins; Staphylococcal Infections; Wound Infection

A newly acquired rhesus macaque was suffering from rapid destruction of the left cheek caused by necrotizing stomatitis.. To restore reconstructive surgery and intensive care with antibiotics, wound protection, wound healing agents, and debridement were applied.. Staphylococcus aureus and Enterococcus faecalis were isolated from the culture of the lesion, and the antibiotic susceptibility test revealed methicillin-resistant Staphylococcus aureus infection. Vancomycin and ampicillin-sulbactam effectively treated the bacterial infections, and reconstructive surgery was performed once the infection was cleared. Topical application of recombinant human epidermal growth factor (rhEGF) was useful to treat exposed wound of the noma lesion.. Simian noma associated with methicillin-resistant Staphylococcus aureus (MRSA) had not previously been reported in non-human primates. Although noma associated with MRSA is hard to cure because of its rapid and destructive progress, the aggressive therapy used in this study led to the successful resolution of an acute necrotic stomatitis lesion in a rhesus macaque.

Topics: Ampicillin; Animals; Anti-Bacterial Agents; Enterococcus faecalis; Epidermal Growth Factor; Gram-Positive Bacterial Infections; Humans; Macaca mulatta; Male; Methicillin-Resistant Staphylococcus aureus; Monkey Diseases; Mouth; Necrosis; Noma; Oral Surgical Procedures; Plastic Surgery Procedures; Staphylococcal Infections; Stomatitis; Sulbactam; Vancomycin; Wound Healing

Local infection of the trachea in intubated neonates is one of the main risk factors for development of acquired subglottic stenosis, although its role in the pathogenesis is unclear. Methicillin resistant Staphylococcus aureus (MRSA) is often the cause of critical illness in neonatal patients. Two cases are reported of acquired subglottic stenosis following bacterial infection of the trachea, suggesting an association with the staphylococcal exotoxin, epidermal cell differentiation inhibitor (EDIN). EDIN-producing MRSA were isolated from purulent tracheal secretions from both infants. Acquired subglottic stenosis in both cases was probably caused by delayed wound healing as the result of EDIN inhibition of epithelial cell migration.

Topics: Epidermal Growth Factor; Female; Humans; Infant, Newborn; Intubation, Intratracheal; Laryngostenosis; Methicillin Resistance; Shock, Septic; Staphylococcal Infections; Staphylococcus aureus; Tracheotomy