46% and 44.59% in the presence of 0.5 mg/ml and 1 mg/ml NAC,

respectively. Discussion NAC is considered a non-antibiotic drug that has anti-bacterial properties. In 1977, Parry and Neu [8] found that NAC had the characteristics to inhibit the growth of both gram-positive and gram-negative bacteria, including S. aureus, P. aeruginosa, K. pneumoniae and Enterobacter clocae. P. aeruginosa was more susceptible than most of the other tested microorganisms (MIC 2-20 μg/ml), P. aeruginosa this website strains were inhibited synergistically by NAC and carbenicillin or ticarcillin. Roberts and Cole [9] found that 2%-5% of NAC was anti-bactericidal against P. aeruginosa, the effect of the carbenicillin on P. aeruginosa was augmented by low concentrations of NAC, and the MIC of the organisms to carbenicillin was reduced from 16 μg/ml to 1 μg/ml in the presence of one per cent NAC. The mechanism for the anti-bacterial effect of NAC may be that it acts by competitively GDC-0449 concentration inhibiting amino acid (cysteine) utilization or, by virtue of possessing a sulfhydryl group, may react with bacterial cell

proteins. Our results are consistent TGFbeta inhibitor with those of Roberts and Cole, as most of the P. aeruginosa strains were inhibited at concentrations < 40 mg/ml of NAC, and a higher percentage of synergistic combinations with NAC was observed with ciprofloxacin (50%). This means that NAC and ciprofloxacin may be used together to treat P. aeruginosa infections. Due to its ability to produce a biofilm, P. aeruginosa is responsible for some chronic pulmonary very infections, such as those in cystic fibrosis (CF), bronchiectasis and chronic obstructive pulmonary disease (COPD).

It also implicates that the infections are associated with endotracheal tubes [10, 11]. P. aeruginosa eventually causes infections in most patients with CF, and once a chronic infection is established, eradication of P. aeruginosa strains is nearly impossible. Patients with bronchiectasis who are colonized by P. aeruginosa exhibit more advanced diseases and more severe impairments of pulmonary function compared with those who remain free of colonization [12–14]. Some observations suggest that P. aeruginosa is a more common cause of infection as COPD advances [15, 16]. Recently, Martínez-Solano et al. [17] showed that patients with COPD were usually infected with at least 1 P. aeruginosa clone that remained in the lungs for years. During chronic infection, each clone diversified, and isolated from samples of infected lungs tended to produce more biofilm compared with the isolation from blood samples. The structure and physiological characteristics of a biofilm confer an inherent resistance to anti-microbial agents. The MICs of anti-microbial agents can be increased 100- to 1000-fold when bacteria grow in biofilms as compared to planktonic bacteria [18]. Therapy almost always fails to eradicate the bacteria in biofilms.