Infection with Helicobacter pylori is a critical cause of gastrointestinal diseases. A crucial host response associated with H. pylori infection includes gastric inflammation, which is characterized by a sustained recruitment of T-helper (Th) cells to the site of infection and distinct patterns of cytokine production. Adequate nutritional status, especially frequent consumption of dietary antioxidants, appears to protect against infection with H. pylori. The aim of the present study was to investigate whether astaxanthin (AXT) from shrimp cephalothorax may modulate cytokine release of splenocytes in H. pylori-infected mice (n = 60). Six- to eight-week-old female mice were divided into three groups (n = 20 per group) to receive a daily oral dose of 10 or 40 mg of AXT for six weeks. After six weeks, a trend toward interferon gamma (IFN-γ) upregulation was found (40 mg; p < 0.05) and a significant dose-dependent increase of interleukin 2 (IL-2) and IL-10 (both p < 0.05) was observed. These results suggest that AXT induces higher levels of IL-2 and a shift to a balanced Th1/Th2 response by increasing IFN-γ and augmenting IL-10. We concluded that AXT may influence the pattern of cytokines during H. pylori infection.

Helicobacter pylori is a common colonizer of the human stomach, and long-term colonization has been related to development of atrophic gastritis, peptic ulcers and gastric cancer. The increased gastric pH caused by H. pylori colonization, treatment with antibiotics or proton pump inhibitors (PPI) may allow growth of other bacteria. Previous studies have detected non-Helicobacter bacteria in stomach biopsies, but no conclusion has been made of whether these represent a transient contamination or a persistent microbiota. The aim of this study was to evaluate the transient and persistent bacterial communities of gastric biopsies. The washed or unwashed gastric biopsies were investigated by cultivation and microbiota analysis (16S rRNA gene-targeted amplicon sequencing) for the distribution of H. pylori and other non-Helicobacter bacteria. The number of cultured non-Helicobacter bacteria decreased in the washed biopsies, suggesting that they might be a transient contamination. No significant differences in the bacterial diversity were observed in the microbiome analysis between unwashed and washed biopsies. However, the bacterial diversity in biopsies shown H. pylori-positive and H. pylori-negative were significantly different, implying that H. pylori is the major modulator of the gastric microbiome. Further large-scale studies are required to investigate the transient and persistent gastric microbiota.

Studies on gastric microbiota find several bacterial families and species in the stomach using molecular-based techniques. When biopsies are cultured, there may be growth of bacteria, pure culture of Helicobacter pylori, or no growth. When looking at the histological sections of corresponding biopsies no bacteria may be seen, except curved rods (H. pylori) adherent to the gastric epithelial cells. In a number of biopsies, several different bacteria are cultured with or without H. pylori. The non–H. pylori bacteria cultured are like the normal oral flora and may be contamination of the samples during endoscopy. In histological sections, these bacteria are seen above the mucin layer and not adherent to the epithelial cells confirming that it is contamination of the samples and can thus not be regarded as gastric microbiota. Therefore, the susceptibility of H. pylori to antibiotics is independent of coexisting bacterial flora. A review of H. pylori susceptibility to antibiotics in untreated and previous treated patients will be given including meta-analyses of H. pylori susceptibility to metronidazole (MTZ), clarithromycin, and levofloxacin. These data indicate that these antibiotics become more doubtful to use for primary therapy and should be banned for secondary therapy without susceptibility testing.

Epsilonproteobacteria is a large group of Gram-negative curved or spiral microaerophilic rods, of which many are difficult to culture. Because this group of bacteria is not very well investigated, our knowledge about them is limited, and a great amount of research is still needed. At least two species are well-established human pathogens: Campylobacter jejuni/coli causing gastroenteritis and Helicobacter pylori causing gastric and extra-gastric manifestations. It is well accepted that H. pylori causes a chronic inflammation in the stomach and thereby causes H. pylori-associated gastritis, which may or may not be symptomatic. The association between H. pylori and peptic ulcers, MALT lymphomas, gastric cancer, idiopathic thrombocytopenic purpura, and unexplained iron-deficiency anemia (IDA) is strongly evidence based. On the other hand, pernicious (vitamin B12 deficiency) anemia, neuromyelitis optica, asthma, and Graves’ disease are less evidence based. H. pylori may also be associated with cardiovascular disease, pancreatitis, pancreatic cancer, obesity, diabetes mellitus type 2, Parkinson’s disease, liver diseases, and preeclampsia. H. pylori is thus involved in many gastric and extra-gastric manifestations either directly or indirectly by several proposed mechanisms including antigenic mimicry.