Alternating portions of high nutrient content in the jejunum and the lower part of the small intestine, where nutrients are less abundant. Under these conditions RelA is likely to be activated, and a temporary increase in ppGpp ensues. Accordingly, EPEC adherence genes are poorly expressed in rich media when ppGpp concentration is low and are activated upon transferring to DMEM. The bacterial growth rates observed in the present study. It has previously been shown that ppGpp enhances the expression of the LEE in enterohemorrhagic E. coli. However, there are some important differences between EPEC and EHEC regarding the expression of the adhesin genes. First, even though both pathotypes share the LEE pathogenicity island, the EAF plasmid is not present in EHEC strains and the LEE genes are thus not regulated by PerC. Second, transcription of the LEE genes in EHEC begins at the mid-exponential phase and peaks at the late exponential/early stationary phase. In contrast, in EPEC the LEE as well as the perABC and bfp operons are maximally activated at the mid-exponential-phase. Third, expression of the LEE genes as well as the adherence capacity of EHEC are higher in LB medium supplemented with bicarbonate, while EPEC neither adhere nor properly expresses the genes associated with adherence when grown in LB supplemented or not with bicarbonate. Even though the environmental conditions required for the synthesis of EPEC and EHEC adherence factors are not identical, ppGpp positively affects the adherence of both lineages. This suggests that regulation by ppGpp is conserved regardless the specific mechanisms of control of adherence employed by the different diarheogenic bacteria. ppGpp is associated with bacterial virulence in several species. In most cases ppGpp plays a positive role and is required to fully induce the virulence genes. For instance in all Proteobacteria hitherto analyzed, such as E. coli, Salmonella enterica, Yersinia pestis, Pseudomonas aeruginosa Francisella tularensis and Bordetella pertusis a positive role for ppGpp was found. This reinforces the notion that upregulation of bacterial virulence by ppGpp is an ancient evolutionary phenomenon. Chronic periodontitis is the most frequent form of periodontitis. The bacterial biofilm is required, but not sufficient, for disease initiation. Major periodontal tissue destruction results from persistent host inflammatory PI-103 PI3K inhibitor immune reaction in response to bacteria. The host inflammatory immune reaction begins when the recognition of the bacterial pathogens occurs by means of antigen-presenting cells, such as dendritic cells. Myeloid DCs, also known as conventional DCs, present a strong capability of capturing antigens, which enables them to stimulate T cells. In this context, in CP, DC activation occurs after coming into contact with lipopolysaccharide or immune complexes produced by periodontal pathogens. In addition, PA-MSHA also resulted in substantial upregulation of CD86 in BMDCs and promoted BMDC maturation. As the whole bacterial PA-MSHA constitutes many potential immunogenic components, further studies are needed to .