Blood leukocyte differential inHelicobacter pylori infection

Karttunen, Tuomo J.; Niemelä, Seppo; Kerola, T

doi:10.1007/bf02088556

Cited by 40 publications

(36 citation statements)

References 21 publications

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“…These findings indicate that H. pylori colonization of the gerbil stomach leads to not only a gastric mucosal inflammatory response but also a systemic response. Previous studies reported that humans infected with H. pylori have significantly higher leukocyte counts than their uninfected counterparts (62,63). The leukocytosis observed in H. pylori-infected gerbils in the current study was substantially greater than the leukocytosis previously observed in H. pylori-infected humans.…”

Section: Discussioncontrasting

confidence: 71%

Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

et al. 2016

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Epidemiologic studies have provided conflicting data regarding an association between Helicobacter pylori infection and iron deficiency anemia (IDA) in humans. Here, a Mongolian gerbil model was used to investigate a potential role of H. pylori infection, as well as a possible role of diet, in H. pylori-associated IDA. Mongolian gerbils (either H. pylori infected or uninfected) received a normal diet or one of three diets associated with increased H. pylori virulence: high-salt, low-iron, or a combination of a high-salt and low-iron diet. In an analysis of all infected animals compared to uninfected animals (independent of diet), H. pylori-infected gerbils had significantly lower hemoglobin values than their uninfected counterparts at 16 weeks postinfection (P < 0.0001). The mean corpuscular volume (MCV) and serum ferritin values were significantly lower in H. pylori-infected gerbils than in uninfected gerbils, consistent with IDA. Leukocytosis and thrombocytosis were also detected in infected gerbils, indicating the presence of a systemic inflammatory response. In comparison to uninfected gerbils, H. pylori-infected gerbils had a higher gastric pH, a higher incidence of gastric ulcers, and a higher incidence of fecal occult blood loss. Anemia was associated with the presence of gastric ulceration but not gastric cancer. Infected gerbils consuming diets with a high salt content developed gastric ulcers significantly more frequently than gerbils consuming a normal-salt diet, and the lowest hemoglobin levels were in infected gerbils consuming a high-salt/low-iron diet. These data indicate that H. pylori infection can cause IDA and that the composition of the diet influences the incidence and severity of H. pylori-induced IDA.A nemia affects up to 1.6 billion people worldwide, potentially resulting in fatigue, decreased productivity, increased susceptibility to infection, or death (1-5). A wide variety of infectious processes can be primary causes of anemia or can exacerbate anemia arising from noninfectious etiologies. For example, intestinal parasitic infections can cause chronic blood loss, leading to iron deficiency anemia (IDA; i.e., anemia due to iron deficiency) (3, 6). Anemia arises in patients with malaria because the parasites invade erythrocytes (2), and bacterial toxins can cause hemolysis (7). In addition, chronic infections, chronic immune activation, and cancer can cause a form of anemia known as "anemia of chronic disease" (8).Colonization of the human stomach with the gastric bacterium Helicobacter pylori is another potential cause of anemia. Anemia often occurs in the setting of symptomatic H. pylori-associated diseases (peptic ulcer disease or gastric cancer), but it has been suggested that H. pylori may also be a cause of IDA in asymptomatic persons with no evidence of peptic ulcer disease or gastric cancer (9). H. pylori has been linked to several other hematologic diseases, including pernicious anemia (vitamin B 12 deficiency arising through an autoimmune-mediated process) and idiopathic throm...

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Section: Discussioncontrasting

confidence: 71%

Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

et al. 2016

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“…There is compelling evidence that basophils and their mediators participate in host defense against parasites (79) and viruses (24,31,32,64). It has been shown that peripheral blood basophils may be increased in H. pylori-positive patients (36). In this study, we provide the first direct evidence that basophils can contribute to H. pylori-induced mucosal inflammation and that a bacterial infection is associated with basophil infiltration.…”

Section: Discussionmentioning

confidence: 59%

“…Thus, H. pylori is involved in mast cell chemotaxis, and activation and release of proinflammatory mediators and cytokines. Although peripheral blood basophils may be increased in H. pylori-positive patients (36), studies of the in vitro effects of H. pylori on histamine release from basophils have yielded inconclusive results (37)(38)(39).…”

mentioning

confidence: 99%

Basophils Infiltrate Human Gastric Mucosa at Sites of Helicobacter pylori Infection, and Exhibit Chemotaxis in Response to H. pylori-derived Peptide Hp(2–20)

Paulis

Prevete

Fiorentino

et al. 2004

The Journal of Immunology

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Basophils, which are normally confined to the circulation, can migrate to sites of allergic inflammation. Using the specific mAb, BB1, we detected basophil infiltration of the gastric mucosa of Helicobacter pylori-infected patients affected by moderate and severe gastritis. Basophils were not found in H. pylori-free individuals or in subjects with mild gastritis. The H. pylori-derived peptide, Hp(2–20), was a potent basophil chemoattractant in vitro, whereas the control peptide, Hp1, was ineffective. Basophils from peripheral blood of healthy volunteers expressed mRNA for the formyl peptide receptors, N-formyl-peptide receptor (FPR), FPR-like (FPRL)1, and FPRL2. Preincubation of basophils with FMLP or Hp(2–20) caused complete desensitization to a subsequent challenge with homologous stimulus. Incubation of basophils with a low concentration of FMLP, which binds with high affinity to FPR, but not to FPRL1 or FPRL2, did not affect the chemotactic response to Hp(2–20). In contrast, a high concentration of FMLP, which binds to FPRL1 and FPRL2, reduced the chemotactic response to Hp(2–20). The FPR antagonist, cyclosporin H, prevented chemotaxis induced by FMLP, but not by Hp(2–20). Hp(2–20) could be responsible, at least in part, for basophil infiltration of the gastric mucosa of H. pylori-infected patients presumably through the interaction with FPRL1 and FPRL2.

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“…Hence, Ig-producing cells should be taken into consideration in the estimation of H. pylori -associated gastric inflammation. Higher peripheral blood leukocyte count [152] and serum levels of anti- H. pylori [153, 154] have also been reported to be associated with increased grading of inflammation, although studies on these factors are limited.…”

Section: Immunoglobulin Production and Othersmentioning

confidence: 99%

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

et al. 2005

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Background: The importance of examining the status of gastric inflammation has been acknowledged; the new classification by the updated Sydney system (USS) allows us to evaluate the quantitative status of gastric inflammation. However, this system is based on the histological classification derived from biopsy specimens. Therefore, more convenient, objective and practical biomarkers are recommended. Aim: We undertook a systematic review to find out potential biomarkers by summarizing the relationship between biomarkers and grades of inflammation. Methods: By a primary search via Medline up to December 2004, we extracted a total of 6,526 papers that described biomarkers for human gastric inflammation. All papers were screened by title and abstract. The authors then retrieved 435 citations for complete review; ultimately 231 were appropriate for inclusion criteria. These papers were subclassified into several categories and summarized by each author. Results: In addition to standard markers such as pepsinogens, we confirmed the close relationship between the levels of several biomarkers including gastrin, interleukin-8, HLA class II molecules, reactive oxygen species, and the histological grades. Conclusions: This review provides valuable information describing the clinical implication of these biomarkers for evaluating the static conditions or dynamic alterations of human gastric inflammation.

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Blood leukocyte differential inHelicobacter pylori infection

Cited by 40 publications

References 21 publications

Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

Dietary Composition Influences Incidence of Helicobacter pylori-Induced Iron Deficiency Anemia and Gastric Ulceration

Basophils Infiltrate Human Gastric Mucosa at Sites of Helicobacter pylori Infection, and Exhibit Chemotaxis in Response to H. pylori-derived Peptide Hp(2–20)

Biomarkers in Patients with Gastric Inflammation: A Systematic Review

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