This review summarizes a collection of lactic acid bacteria that are now undergoing genomic sequencing and analysis. Summaries are presented on twenty different species, with each overview discussing the organisms fundamental and practical significance, environmental habitat, and its role in fermentation, bioprocessing, or probiotics. For those projects where genome sequence data were available by March 2002, summaries include 30 a listing of key statistics and interesting genomic features. These efforts will revolutionize our molecular view of Gram-positive bacteria, as up to 15 genomes from the low GC content lactic acid bacteria are expected to be available in the public domain by the end of 2003. Our collective view of the lactic acid bacteria will be fundamentally changed as we rediscover the relationships and capabilities of these organisms through genomics.

In this study, we investigated the agrBDCA operon in the pathogenic bacterium Listeria monocytogenes EGD-e. In-frame deletion of agrA and agrD resulted in an altered adherence and biofilm formation on abiotic surfaces, suggesting the involvement of the agr system of L. monocytogenes during the early stages of biofilm formation. Real-time PCR experiments indicated that the transcript levels of agrBDCA depended on the stage of biofilm development, since the levels were lower after the initial attachment period than during biofilm growth, whereas transcription during planktonic growth was not growth phase dependent. The mRNA quantification data also suggested that the agr system was autoregulated and pointed to a differential expression of the agr genes during sessile and planktonic growth. Although the reverse transcription-PCR experiments revealed that the four genes were transcribed as a single messenger, chemical half-life and 5 RACE (rapid amplification of cDNA ends) experiments indicated that the full size transcript underwent cleavage followed by degradation of the agrC and agrA transcripts, which suggests a complex regulation of agr transcription.Listeria monocytogenes is a gram-positive human pathogenic bacterium; it is the causative agent of listeriosis, a serious infection characterized by high mortality rates, in immunocompromised individuals and pregnant women (19). This pathogenic bacterium is widely spread in the environment (soil, vegetation, animals, farm environment, etc.). In connection with these extended reservoirs, L. monocytogenes is also a contaminant of the food industry. Its presence on working surfaces in food-processing plants is a major problem as a source of food contamination (1, 32). Like most bacteria, L. monocytogenes is able to colonize surfaces and form biofilms (sessile growth) while, in natural environments, free-floating cells (planktonic growth) are transitory (28). Several steps can be identified during biofilm development: after an initial step of reversible and then irreversible adherence, bacteria grow as microcolonies and spread on the surface. Finally, biofilms develop as complex, three-dimensional structures during the maturation step (17). Biofilm development and maturation requires complex cellular mechanisms in which cell-cell communication is involved (14, 30). To date, three major signaling systems have been identified; to regulate these systems, bacterial extracellular signaling molecules called autoinducers are produced (8). The acylhomoserine lactones have been identified as autoinducers in gram-negative bacteria (3, 13, 27, 46). The autoinducer 2 is found in both gram-negative and gram-positive bacteria (5,7,11,35,36,54). Finally, peptide-mediated signaling pathways have been characterized in gram-positive bacteria. Among these, the agr system has been described initially in Staphylococcus aureus (41); the production of many of its virulence factors (toxins, enzymes, and cell surface proteins) is regulated by this system (4). The role of the agr system during ...

A PCR-restriction fragment length polymorphism (RFLP) method was developed in order to screen a large number of strains for impaired adhesion to epithelial cells due to expression of truncated InlA. inlA polymorphism was analyzed by PCR-RFLP in order to correlate inlA PCR-RFLP profiles and production of truncated InlA. Thirty-seven Listeria monocytogenes strains isolated from various sources, including five noninvasive and two invasive reference strains, were screened. Two endonucleases (AluI and Tsp509I) were used, and they generated five composite profiles. Thirteen L. monocytogenes isolates were characterized by two specific PCR-RFLP profiles similar to PCR-RFLP profiles of noninvasive reference strains previously described as strains that produce truncated InlA. Ten of the 13 isolates showed low abilities to invade human epithelial Caco-2 cells. However, 4 of the 13 isolates were able to invade Caco-2 cells like reference strains containing complete InlA. Sequencing of inlA and Western blot analysis confirmed that truncated InlA was expressed in the 10 L. monocytogenes strains which were isolated from food. This PCR-RFLP method allowed us to identify 10 new strains expressing a truncated internalin. Based on the results obtained in this study, the PCR-RFLP method seems to be an interesting method for rapidly screening L. monocytogenes strains deficient in the ability to invade Caco-2 cells when a sizeable number of strains are studied.

No abstract

Autophagy is an intracellular catabolic pathway essential for the recycling of proteins and larger substrates such as aggregates, apoptotic corpses, or long-lived and superfluous organelles whose accumulation could be toxic for cells. Because of its unique feature to engulf part of cytoplasm in double-membrane cup-shaped structures, which further fuses with lysosomes, autophagy is also involved in the elimination of host cell invaders and takes an active part of the innate and adaptive immune response. Its pivotal role in maintenance of the inflammatory balance makes dysfunctions of the autophagy process having important pathological consequences. Indeed, defects in autophagy are associated with a wide range of human diseases including metabolic disorders (diabetes and obesity), inflammatory bowel disease (IBD), and cancer. In this review, we will focus on interrelations that exist between inflammation and autophagy. We will discuss in particular how mediators of inflammation can regulate autophagy activity and, conversely, how autophagy shapes the inflammatory response. Impact of genetic polymorphisms in autophagy-related gene on inflammatory bowel disease will be also discussed.