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Helicobacter pylori (H. pylori) is a successful pathogen that can persist in the stomach of an infected person for their entire life. It provokes chronic gastric inflammation that leads to the development of serious gastric diseases such as peptic ulcers, gastric cancer and Mucosa associated lymphoid tissue lymphoma. It is known that these ailments can be avoided if the infection by the bacteria can be prevented or eradicated. Currently, numerous antibiotic-based therapies are available. However, these therapies have several inherent problems, including the appearance of resistance to the antibiotics used and associated adverse effects, the risk of re-infection and the high cost of antibiotic therapy. The delay in developing a vaccine to prevent or eradicate the infection has furthered research into new therapeutic approaches. This review summarises the most relevant recent studies on vaccine development and new treatments using natural resources such as plants, probiotics and nutraceuticals. In addition, novel alternatives based on microorganisms, peptides, polysaccharides, and intragastric violet light irradiation are presented. Alternative therapies have not been effective in eradicating the bacteria but have been shown to maintain low bacterial levels. Nevertheless, some of them are useful in preventing the adverse effects of antibiotics, modulating the immune response, gastroprotection, and the general promotion of health. Therefore, those agents can be used as adjuvants of allopathic anti-H. pylori eradication therapy.

Escherichia coli R170, isolated from the urine of an infected patient, was resistant to expanded-spectrum cephalosporins, aztreonam, ciprofloxacin, and ofloxacin but was susceptible to amikacin, cefotetan, and imipenem. This particular strain contained three different plasmids that encoded two ␤-lactamases with pIs of 7.0 and 9.0. Resistance to cefotaxime, ceftazidime, aztreonam, trimethoprim, and sulfamethoxazole was transferred by conjugation from E. coli R170 to E. coli J53-2. The transferred plasmid, RZA92, which encoded a single ␤-lactamase, was 150 kb in length. The cefotaxime resistance gene that encodes the TLA-1 ␤-lactamase (pI 9.0) was cloned from the transconjugant by transformation to E. coli DH5␣. Sequencing of the bla TLA-1 gene revealed an open reading frame of 906 bp, which corresponded to 301 amino acid residues, including motifs common to class A ␤-lactamases:70 SXXK, 130 SDN, and 234 KTG. The amino acid sequence of TLA-1 shared 50% identity with the CME-1 chromosomal class A ␤-lactamase from Chryseobacterium (Flavobacterium) meningosepticum; 48.8% identity with the VEB-1 class A ␤-lactamase from E. coli; 40 to 42% identity with CblA of Bacteroides uniformis, PER-1 of Pseudomonas aeruginosa, and PER-2 of Salmonella typhimurium; and 39% identity with CepA of Bacteroides fragilis. The partially purified TLA-1 ␤-lactamase had a molecular mass of 31.4 kDa and a pI of 9.0 and preferentially hydrolyzed cephaloridine, cefotaxime, cephalothin, benzylpenicillin, and ceftazidime. The enzyme was markedly inhibited by sulbactam, tazobactam, and clavulanic acid. TLA-1 is a new extended-spectrum ␤-lactamase of Ambler class A.The main mechanism of resistance to ␤-lactam antibiotics in members of the family Enterobacteriaceae is the production of ␤-lactamases (21, 35). Expanded-spectrum cephalosporins (cefotaxime, ceftazidime) have been specifically designed to resist degradation by the older broad-spectrum ␤-lactamases such as TEM-1, TEM-2, and SHV-1. With the use of these antibiotics in vivo, extended-spectrum ␤-lactamases (ESBLs) have been selected; these ESBLs most often are mutants of these older enzymes and carry a limited number of amino acid substitutions (G. Jacoby and K. Bush, http://www.lahey.org/studies /webt.htm). There is also a small but growing family of plasmid-mediated ESBLs that are not related to TEM or SHV ␤-lactamases, such as 10,14,15) and Toho (17,23), that preferentially hydrolyze cefotaxime and that belong to Ambler class A. In addition, there has been a worldwide emergence of novel ␤-lactamases, mainly among members of the family Enterobacteriaceae, that hydrolyze expanded-spectrum ␤-lactams. While they maintain the main properties of the class A ␤-lactamases, they are not closely related to the TEM, SHV, or CTX-M families of ␤-lactamases. Most of these ESBLs are plasmid mediated and include the PER-1, PER-2, VEB-1, CblA, and CepA enzymes. These ␤-lactamases are not species specific, since they have also been isolated from clinically significant gram-negative species that are not mem...

We describe, for the first time, the ability of a polyoxyethylene sorbitan trioleate-isopropanol microemulsion in hexane to solubilize pure proteins. The dependences of cytochrome c extraction and buffer solubilization by the reverse micellar system on ionic strength of the aqueous phase, detergent concentration, and cosurfactant concentration result in increased extraction. In addition, subtilisin (a serine protease) is shown to be active in this microemulsion. Further the activity of the enzyme can be regulated by the water content of the micelles, enabling control of enzyme activity by "solvent engineering."

The Helicobacter pylori infection of gastric mucosa is one of the most common infectious diseases and is associated with a variety of clinical outcomes, including peptic ulcer disease and gastric cancer. Helicobacter pylori-induced damage to gastric mucosal cells is controlled by bacterial virulence factors, which include VacA and CagA. Outer membrane vesicles are constantly shed by the bacteria and can provide an additional mechanism for pathogenicity by releasing non-secretable factors which can then interact with epithelial cells. The present report shows that external membrane vesicles are able to induce apoptosis not mediated by mitochondrial pathway in gastric (AGS) epithelial cells, as demonstrated by the lack of cytochrome c release with an activation of caspase 8 and 3. Apoptosis induced by these vesicles does not require a classic VacA+ phenotype, as a negative strain with a truncated and therefore non-secretable form of this protein can also induce cell death. These results should be taken into account in future studies of H. pylori pathogenicity in strains apparently VacA-.

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