Abstract
Infections by Streptococcus pneumoniae are a major cause of morbidity and mortality worldwide, often causing community-acquired pneumonia, otitis media and also bacteremia and meningitis. Studies on S. pneumoniae are mainly focused on its virulence or capacity to evade the host immune system, but little is known about the injury caused in lungs during a pneumococcal infection. Herein we investigated this issue comparing the proteome profile of lungs from S. pneumoniae-infected mice with control mice by means of difference gel electrophoresis (DIGE) technology. In order to obtain reliable results three biological replicas were used, and four technical replicas were carried out in each biological replica. Proteomic comparison was performed at two time points: 24 and 48 h post infection. A total of 91 proteins were identified with different abundance. We found important changes in the protein profiles during pneumococcal infection mainly associated with regulation of vesicle-mediated transport, wound healing, and cytoskeleton organization. In conclusion, the results obtained show that the cytoskeleton of the host cell is modified in S. pneumoniae infection.
Highlights
Since the isolation of Streptococcus pneumoniae in 1881 these bacteria have been one of the most extensively studied human pathogens
Balb/c mice were intranasally inoculated with either 5 × 107 colony forming units (CFU) of S. pneumoniae TIGR4 or with phosphatebuffered saline (PBS) as a mock treatment, and disease progression was evaluated by body weight loss, granulocyte/lymphocyte ratio in blood and bacterial loads in the lungs, blood, and systemic organs
Significant body weight loss was already observed in S. pneumoniaeinfected mice 24 h after inoculation compared to PBS-treated animals, being even more pronounced at 48 h after treatment (Figure 1A)
Summary
Since the isolation of Streptococcus pneumoniae in 1881 these bacteria have been one of the most extensively studied human pathogens. The Bottomup approach begins with the enzymatic digestion of proteins into peptides that are separated, identified, or quantified by mass spectrometry. Different studies have employed different proteomic approaches in order to identify changes in protein abundance in the host during infection. To carry out this study we used the TIGR4 strain of S. pneumoniae This strain is a highly virulent capsular serotype 4 clinical isolate obtained from the blood of a 30-year-old male patient in Kongsvinger, Norway (Aaberge et al, 1995). The genome of this strain was described in Tettelin et al (2001). The TIGR4 isolate was previously reported as JNR.7/87, the label of the clinical isolate (Bricker and Camilli, 1999), but it can be found in the literature as KNR.7/87 (de Saizieu et al, 2000); and as N4 (Wizemann et al, 2001)
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