# _Helicobacter pylori_--The Bridge between Local and Systemic Inflammation in Children
###### Abstract  
_Helicobacter pylori_ (_H. pylori_)-associated inflammatory status is no longer a debatable topic in children. The aim of our study was to to compare the inflammatory status in pediatric patients with _H. pylori_ gastritis and non-_H. pylori_ gastritis versus control group. We performed a prospective study on 68 children with dyspptic symptoms which were divided into 3 groups: 14 children with _H. pylori_ gastritis (group 1), 26 children with non-_H. pylori_ gastritis (group 2) and 28 children with no pathological findings--control group (group 3). Several laboratory parameters, histopathological and immunohistochemistry tests were performed in all children for detecting inflammatory status. We noticed a significant difference in terms of rural area between the three groups (_p_ = 0.0404). Comparing the laboratory parameters between the three groups, we noticed significant differences in terms of serological tests (_p_ = 0094), and NLR (_p_ = 0.0253), the latter being significantly higher in children with _H. pylori_-induced gastritis as compared to those with non-_H. pylori_ gastritis (0.0107). According to the Dunn's Multiple Comparison Test, we noticed a significantly elevated neutrophil level in children with _H. pylori_-induced gastritis when compared to non-_H. pylori_ gastritis group (_p_ = 0.0146), as well as a significantly increased eosinophil count in patients with non-_H. pylori_ gastritis as compared to control group (_p_ = 0.0417). The immunohistochemistry method pointed out no significant variation concerning interleukin (IL 6) between children with gastritis and control group [RR = 1.283, IC (95%): 0.9404-1.751, \(p\) = 0.0988]. Additionally, children with gastritis regardless of the etiology have a significant risk of associating increased gastric expression of tumor necrosis factor alpha (TNF \(\alpha\)) [RR = 3.967; CI (95%): 1.283-12.263; \(p\) = 0.0063]. Moreover, TNF \(\alpha\) was significantly associated with presence of _H. pylori_ gastritis (_p_ = 0.0002). The early detection of local inflammation triggered by this infection might preempt gastric carcinogenesis, while identifying _H. pylori_-induced systemic inflammation lowers the risk of severe extraintestinal manifestations. Helicobacter pylori; systemic inflammation; gastritis; children 202313216202313216202313216202313216202313216202316202313216202316202  
ulcer, gastric malignancies, iron deficiency anemia, vitamin B deficiency, thrombocytopenia purpurura, growth deficiency, and less common cardiovascular diseases, diabetes mellitus, insulin resistance, obesity, autoimmune, ophthalmic, neurological or dermatological conditions [1; 2]. In terms of gastric carcinogenesis, _H. pylori_ has been well-documented to be involved in 80% of all gastric cancers and more than 5% of all malignancies worldwide resulting in aggressive tumors such as gastric-associated lymphoid tissue lymphoma or gastric adenocarcinomas [3; 4]. Although the local damage caused by _H. pylori_ is related especially to its virulence characteristics such as lipopolysaccharideaccharides, flagellin, cag-pathogenicity island, pathogen-associated molecular patterns, vacuolating cytotoxin A, and adhesins [5], the systemic negative impact seems to be related to the host's innate and adaptive immunity which contributes to the development of subclinical systemic inflammation [6]. Thus, the host's immune system owns a major role in triggering the wide-spectrum of extraintesinal manifestations that were suggested to be related to the presence of this bacterium at the level of the gastric mucosa [2]. Surprisingly, while gastric carcinogenesis is a complex process which requires a considerable amount of time for its development, most of the extraintesinal manifestations were reported even in pediatric patients [7] proving once more that the occurrence of the so-called devastating systemic subclinical inflammation might not depend on the length of this infection, but on relationship between the host and the bacterium itself.