We developed and evaluated a recombinant Borrelia line immunoblot assay based on 18 homologues of seven different antigens, i.e., p100, p58, p41i, BmpA, VlsE, OspC, and DbpA. Each recombinant antigen can be detected separately and is distinct even from homologues with identical molecular weights. This blot was compared to the recently described recombinant Borrelia Western immunoblot assay (U. Schulte-Spechtel, G.

Alteration of the outer surface protein (Osp) composition -especially that of OspA and OspC -seems to be important for the adaptation of Borrelia burgdorferi sensu lato to its endothermic hosts (mammals) and poikilothermic vectors (ticks). OspA possibly mediates adherence to tick midgut cells thus enabling the borreliae to survive in the vector, while OspC is associated with borrelial invasion of the tick salivary glands and infection of the mammalian hosts. Here we describe the first successful transformation and complementation of a Borrelia afzelii ospC mutant with the wild-type ospC in trans. To test the influence of OspC on the dissemination behavior in ticks, unfed Ixodes ricinus nymphs were artificially infected by capillary feeding either with B. afzelii wild type, the B. afzelii ospC mutant or the ospC-complemented clone. Tick midguts and salivary glands were investigated after different time intervals for the presence of borreliae and for OspA and OspC by immunfluorescence staining with monoclonal antibodies. While the B. afzelii wild-type strain exhibiting abundant OspC on its surface disseminated to the salivary glands, the OspCnegative mutant was only present in the tick midguts. The ospC-complemented clone which constitutively expresses the wild-type ospC was again able to colonize the salivary glands. This finding demonstrates that OspC is crucial for dissemination of B. afzelii from the tick midgut to the salivary glands, a prerequisite for infection of the warm-blooded host. A summary of the detailed data presented here has already been given in Goettner et al.

Helicobacter pylori-specific proteins are involved in gastric carcinogenesis. To investigate the seroprevalence of six H. pylorispecific antibodies in patients with different gastric histology, and the impact of seropositivities on the evolution of precancerous gastric lesions, a follow-up study was conducted in Linqu County, China. The seropositivities for CagA, VacA, GroEL, UreA, HcpC and gGT were assessed by recomLine analysis in 573 H. pylori-positive subjects and correlated with evolution of precancerous gastric lesions. We found that the score of H. pylori recomLine test was significantly increased in subjects with chronic atrophic gastritis (CAG, p < 0.0001) or intestinal metaplasia (IM, p 5 0.0125), and CagA was an independent predictor of advanced gastric lesions, adjusted odds ratios (ORs) were 2.54 (95% CI 5 1.42-4.55) for IM and 2.38 (95% CI 5 1.05-5.37) for dysplasia (DYS). Moreover, seropositivities for CagA and GroEL were identified as independent predictors for progression of gastric lesions in a longitudinal study, and ORs were 2.89 (95% CI 5 1.27-6.59) and 2.20 (95% CI 5 1.33-3.64), respectively. Furthermore, the risk of progression was more pronounced in subjects with more than three positive antigens (p for trend 5 0.0003). This population-based study revealed that seropositivities for CagA and GroEL might be potential markers to identify patients infected with high-risk H. pylori strains, which are related to the development of GC in a Chinese high-risk population, and recomLine test might serve as a tool for risk stratification.Helicobacter pylori (H. pylori) is a Gram-negative bacterium identified as the strongest known risk factor for gastric cancer (GC). 1 H. pylori infection can induce chronic gastritis, persisting for decades and eventually progressing to chronic atrophic gastritis (CAG), intestinal metaplasia (IM), dysplasia (DYS) and GC. 2,3 Our two randomized, placebo-controlled factorial-design intervention trials in Linqu County, a highrisk area of GC in Shandong Province, China, indicated that H. pylori eradication significantly reduces the risk of precancerous gastric lesions and subsequent GC, [4][5][6] suggesting that H. pylori eradication could be an effective strategy to prevent GC.However, although about half of the world's population is infected with H. pylori, only a minority of infected subjects

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