ABSTRACT
Studies have demonstrated that heat shock protein 70 (HSP70) plays an important role in the protection of stressed organisms. The development of strategies for enhancing HSPs expression may provide novel means of minimizing inflammatory lung conditions, such as acute lung injury. This study aimed to examine the effect of L-alanyl-L-glutamine (GLN) inhalation in enhancing pulmonary HSP72 (inducible HSP70) expression and attenuating lung damage in a model of acute lung injury induced by lipopolysaccharide (LPS) inhalation. The experimental rats were randomly assigned to one of four experimental groups: (1) NS: saline inhalation; (2) NS-LPS: pretreatment by saline inhalation 12 h before LPS inhalation; (3) GLN: glutamine inhalation; (4) GLN-LPS: pretreatment by glutamine inhalation 12 h before LPS inhalation. The results show that GLN compared with saline administration, led to significant increase in lung HSP72 both in non LPS-treated rats and LPS-treated rats. In LPS-treated rats, pretreatment by GLN inhalation produced less lung injury as evidenced by the decrease in lung injury score and dramatic decrease in lactate dehydrogenase (LDH) activity and polymorphonuclear leukocyte cell differentiation counts (PMN %) in the bronchoalveolar lavage fluid. The study indicates that prophylactic glutamine inhalation associated with the enhancement of HSP72 synthesis attenuates tissue damage in experimental lung injury.
Subject(s)
Dipeptides/administration & dosage , HSP72 Heat-Shock Proteins/metabolism , Lung Injury/metabolism , Lung Injury/prevention & control , Lung/metabolism , Administration, Inhalation , Animals , Dose-Response Relationship, Drug , Lipopolysaccharides , Lung/drug effects , Lung Injury/complications , Male , Rats , Rats, Sprague-Dawley , Treatment OutcomeABSTRACT
Enterococci might be one of the meningitis pathogens, but meningitis is rarely caused by vancomycin-resistant enterococci. In this report, we present a 69-year-old man who had the underlying chronic obstructive pulmonary disease with long-term steroid treatment suffered from a meningitis episode after hospitalisation for the urinary tract infection. The cerebrospinal fluid culture of the patient grew Enterococcus faecium which was resistant to vancomycin. A vancomycin-resistant E. faecium was also isolated from the rectal swab of the patient. These two E. faecium isolates were found to harbour the vanA gene and to be identical by pulsed field gel electrophoresis typing. The patient was treated successfully with intravenous linezolid, 600 mg every 12 h for 2 weeks. This was the first case of meningitis caused by vancomycin-resistant E. faecium in Taiwan.
