**3. Liver injury**

In developed countries, infection by these bacteria is detected in about 50% of the population, while in developing countries, the percentage may even reach 90% [2]. Still, however, there

*H. pylori* produces high amounts of ureases, enzymes catalyzing urea decomposition to ammonia. This is especially important for the neutralization of hydrochloric acid in the stomach, which contributes to the growth of the bacteria. Bacteria demonstrate also the ability to

*H. pylori* has an active antioxidizing system, which neutralizes free radicals. The system con-

Bacterial DNA contains genes encoding cytotoxin synthesis system. VacA toxin (vacuolating toxin) is encoded by a changing system of genes in 40–60% of bacterial strains. This underlies different toxic properties. In epithelial cells, VacA promotes fusion of several lysosomes and formation of large vacuoles, which changes the construction of cytoskeleton. VacA toxin

Specific system of CagA genes encodes synthesis of CagA toxin, demonstrating properties reorganizing cytoskeleton and cell shape. Moreover, the toxin controls transcription and proliferation of the cell, as well as inflammatory reaction. CagA toxin plays a very important role in carcinogenesis in the stomach and other organs, when CagA-synthesizing *H. pylori* is detected [3, 4].

*H. pylori* is mainly present on the surface of epithelial cells of the mucosa, in the prepyloric part of the stomach. It has cilia allowing transport into intercellular spaces, and thanks to

*H. pylori* infection influences local (in the gastric mucosa) and systemic increase in proinflammatory cytokines IL-1, -2, -4, -6, -8, -10, -17, interferon-β, and TNF-α [5]. This leads not only to development of local inflammatory reaction, but also potentiates generalized inflammatory reactions in the organism. *H. pylori* causes chronic atrophic gastritis, metaplasia, and dysplasia, leading to the development of gastric cancer. According to World Health Organization (WHO), the bacteria are a class I carcinogen. *H. pylori* may also potentiate extragastric organ disturbances, exacerbating the diseases of cardiovascular system or metabolic diseases, dete-

*H. pylori* infection, especially in the case of strains producing CagA toxin, promotes development of coronary sclerosis and increases the probability of angina pectoris and cardiac infarct [7]. Effect of CagA toxin on promotion of sclerotic changes in coronary arteries leads to exacerbation of coronary disease, which increases mortality caused by circulatory failure in the group of patients infected with these bacteria and not subjected to eradication [8, 9].

*H. pylori* infection among patients with type 2 diabetes presents more seriously compared to patients without diabetes [10]. Moreover, impact of this infection onto the development of

chronic pancreatitis has been reported, which indirectly affects liver function [11].

tains catalase, superoxide dismutase, and specific proteins MdaB and NapA.

induces apoptosis of epithelial cells and shows highly immunogenic properties.

riorating normal function of the liver, especially in patients with cirrhosis [6].

**2. Organ pathologies connected with** *H. pylori* **infection**

ions from cells. This leads to changes in the pH in the stomach, which in turn

are no definitive pointers as to risk factors of *H. pylori* infection.

48 Helicobacter Pylori - New Approaches of an Old Human Microorganism

pump out H<sup>+</sup>

causes destruction of gastric mucosa.

produced adhesins, it adheres to cell surface [1].

Liver colonization by *H. pylori* happens after transmission of the bacteria from the stomach, with blood, through the portal vein or directly through the bile ducts [13].

Experimental studies performed on mice and rats infected with *H. pylori* have shown the effect of this infection onto up triggered fibrosis and development of liver cirrhosis [14]. One of the first studies performed in patients with chronic liver injury pointed to the presence of *Helicobacter* genus bacteria in the liver tissue in 26% of patients [15]. Current studies in patients infected with HBV, HCV, and patients with chronic noninfectious liver conditions point to much higher incidence of *H. pylori* or bacterial DNA in the liver tissue. Infections are thought to occur in effect of disturbances in patients' immune functions [16]. Both experimental and clinical studies demonstrate unfavorable effect of *H. pylori* infection onto the course of liver injury, especially exacerbated fibrosis. One of the reasons for this is the influence of infection onto metabolic changes connected with carbohydrate turnover, synthesis of highenergy compounds (mainly ATP), and increased concentration of proinflammatory cytokines.
