Helicobacter pylori (H. pylori) was cultured for the first time by Warren and Marshall in 1983(1). Since that time, it has been recognized as one of the most common infections in the world and it is accepted as a cause of type B gastritis and duodenal and gastric ulcer as well as a risk factor for gastric cancer (2). The route of H. pylori transmission, its natural history after initial infection, and factors defining disease severity are currently being investigated. A wide geographical variety of H. pylori prevalence has been reported, with high levels in developing countries and lower rates in developed countries (3), in particular between different ethnic groups (4). Reasons for the ethnic predilection are not entirely clear. Genetic factors may account for these differences (5). Ethnic differences may also be a surrogate marker for different environmental exposures within the community. Low socioeconomic status and crowded living conditions commonly associated with poor hygienic conditions have been suggested as major risk factors facilitating H. pylori infection in less developed countries. However, the high variations within and between these countries implies that certain socio-cultural practices influence infection to some extent.

Antrum biopsies from 45 H. pylori-positive patients were selected from the pathology archive at kKing Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia in three consecutive months. The hematoxylin eosin stain preparations of each patient were reviewed and the values obtained by selection of the cases that have severe helicobacter intensity and less intense inflammatory reaction ( group 1), the cases that have a direct relationship between the intensity of helicobacter and intensity of inflammatory reaction, ( group 2), and cases that show intense inflammatory reaction and less helicobacter intensity (group 3). Every slide is examined at scan power view 4X, 10X, and at high power view 20X, 40X.

Aim of the work. The aim of this study was to investigate the relationship between severity of inflammatory reaction in gastritis and intensity of Helicobacter pylori in the antrum by studying the cases of antral gastritis positive for helicobacter bacilli sent to the pathology laboratory in King Khalid University Hospital within 3 consecutive months. Tthe number of cases positive for Helicobacter were 45 cases. 18 of these were female and 27 of were male . In this study it was noticed that the severity of the bacterial infection detected by the number of foveolar involvement and number of bacilli present within the foveola and mucosal surface is not always correlated with inflammatory reaction presented by the amount of inflammatory cells lymphocytes and plasma cells in the lamin propria and the signs of reactivity in the form of infiltration of the glands and lamina propria by polymorphonuclear leukocytes .

The results were as follows:

1. Group 1: 15 cases show a mild reaction in the form of few lymphocytes and plasma cells with rare neutrophilic infiltration of the glands associated with a large amount of helicobacter in the form of increased number of bacilli and the number of foveolae involved . (Fig 1,2,3 and 4)
2. Group 2: 10 cases show a correlation between the amount of helicobacter bacilli (number of the bacillus and number of foveolae involved. Most of the these cases are of moderate degree of inflammatory reaction and moderate amount of helicobacter bacilli. (Fig. 5, 6 and 7)
3. Group 3: 20 cases show a severe type of inflammatory reaction and activity with lymphoid follicle formation in some of them and polymorph within lamina propria and infiltrating glands, but the amount of helicobacter range from minimal in number of bacilli and number of foveolar involvement to very rarely and difficult to find bacilli but it is present. (Fig. 8, 9 and 10)

Throughout the world, the rate of Helicobacter pylori infection increases with age (6). In the stomach, it induces significant cellular and humoral immune responses via the antigenic stimulus of mucosal monocytes and T-lymphocytes. Various cytokines, proteases, prostaglandins, and reactive O2 metabolites released from these inflammatory cells increase the endothelial adhesion of neutrophilic leukocytes. Local humoral mediators such as mucosal IgA lead to leukocyte accumulation, and the degranulation of eosinophilic leukocytes brings about the secretion of various cytokines, contributing to the progress of tissue damage (6).

While it is known that humans serve as the natural host of H. pylori, the exact mechanism of transmission is still unclear. Most researchers believe that infection occurs via oral-oral (kissing) or fecal-oral (food or water contamination) transmission. (7) In the United States only 20 percent of the population under 40 years of age is infected. But since infection continues to spread with time, the rate grows with each passing year until 50 percent of all US citizens over the age of 60 are infected. The infection problem is even greater outside of the US, with infection beginning early in childhood, leading to adult rates of infection approaching 90 percent in some parts of Asia and Africa. (8)

In this study group 2 represented by the 10 patients, the amount of bacilli correlate with the severity of inflammatory reaction determined that the severity of infection is important enough to manifest the gastritis, as presented by the severity of inflammatory reaction. The other two groups go against this theory as regards the 20 cases (in group 3) in which the inflammatory reaction is too much to be explained by the low amount and number of helicobacter pylori found within the tissue and glands. In the other 15 cases ( group 1) the opposite is shown - in which the number and amount of helicobacter presented and number of foveola involved, are not explained by the amount of inflammatory reaction noticed in these cases. Additionlythe activity of the inflammatory reaction presented as neutrophilic infiltrate within lamina propria and glands, were noticed in most or all of the cases ranging from mild to moderate and rarely severe. The presence of eosinophils were noticed in most of the cases. This means that there were probably different responses which depend on interactions between the bacteria and host factors (9). Other factors may play a role in the host tissue response against the Helicobacter pylori infection. These factors may be the virulence of the organism and its strain and, mast cells (10). There are many studies investigating the relationship between H. pylori infection in childhood and symptoms of abdominal pain in selected and unselected populations(11-13). These studies showed that H. pylori infection in childhood was mostly asymptomatic and not associated with specific gastrointestinal symptoms(11-12). In our study group 1the amount of the bacilli were intense and not correlated with the tissue reaction and may lead to the possibility of a carrier status of the host whocarries the bacilli in large amounts but show no symptoms on clinical presentation and this could be a source of infection, There are some studies investigating the possible protective role of breastfeeding against H. pylori infection (14,15,16). Anti-H. pylori IgA in human breast milk has been shown to protect against early acquisition of H. pylori infection in developing countries [15]. Malaty et al.[16] found that breastfeeding had a significant protective effect against acquiring the infection in children. On the other hand, McCallion et al (14) were not able to show the protective role of breastfeeding against H. pylori infection, but they concluded that breastfeeding might reduce the risk of infection. In our study this different tissue reaction could be explained by a difference in the immune response of the host. Alsogenetic factors and family predisposition could play a role in the tissue response to helicobacter pylori as shown by Drumm et al (17) in which family members of 34 children who were diagnosed to have H. pylori gastritis by upper gastrointestinal were investigated by endoscopy. They found that the sero-prevalence of H. pylori was 73.5% in family members of the study group. This study showed that intra-familial clustering of H. pylori infection might be an important risk factor for the spread of infection to the children.

There have been several studies done in Turkish children whose families migrated to Germany before or after their birth, investigating the prevalence and associated risk factors for H. pylori infection (18-19). The prevalence of H. pylori infection is very high among adults in Turkey. There are data on the prevalence of H. pylori infection in children of Turkish immigrants living in different parts of Europe, however, there is limited knowledge on the prevalence, determinants and associations of H. pylori infection among healthy Turkish children living in their native country (18, 20, 21).

Also H. pylori defends itself from another immune threat - the human immune system. The immune inflammatory response involves the production of vast numbers of neutrophils that are mobilized to destroy invading pathogens. Safely ensconced behind its mucus and antacid barriers, H. pylori is protected from attack by the immune system which cannot penetrate the mucus lining. Additionally, H. pylori produces another enzyme called catalase that further protects the bacteria from neutrophils. The result is that instead of repelling H. pylori, the immune inflammatory response causes severe damage to the stomach lining, thus contributing to gastritis and ulcer formation. (22) These can explain the variability of inflammatory reaction as a response to helicobacter, and may be caused by familial issues such as diet, that may be rich in antioxidants in some of these patient and this antioxidants can neutralize the free radicals produced by the inflammatory cells. So we can conclude that the inflammation that occurs in gastritis is not related to the amount of the microorganisms by a direct relationship, but may be related to the quantity of the mediators that are produced by the inflammatory cells that can produce chemotactic effects to the lymphocytes and plasma cells.

The aim of this study was to investigate the relationship between, Helicobacter pylori intensity and histopathological severity of gastritis in the antrum mucosa.

Methods: The study included 45 Helicobacter pylori-positive patients. All cases underwent histopathological examination. All cases were evaluated. The comparision between Helicobacter pylori intensity and histopathological severity of gastritis in the antrum mucosa wasinstituted.

Results: in the antrum the intensity of helicobacter pylori and the intensity of inflammatory reaction in some cases are correlated, but in most of the cases there was a variability in the degree of intensity of helicobacter and that of inflammatory reaction

Conclusions: In the light of the results of our study, it is suggested that there are other factors that play a role in the development of Helicobacter pylori gastritis. These factors may be the mediators that are produced by the inflammatory cells, which can be neutralized by a diet rich in antioxidants.