Antibodies to human gastric epithelial cells and heat shock protein 60 in Helicobacter pylori positive mucosa associated lymphoid tissue lymphoma

Kawahara, Yoshiro; Yokota, Kenji; Mizuno, Motowo; Yunoki, Naoko; Uesu, Tokurou; Okada, Hiroyuki; Kobayashi, Keita; Hirai, Yoshikazu; Oguma, Keiji; Tsuji, Takao

doi:10.1136/gut.45.1.20

Cited by 48 publications

(35 citation statements)

References 17 publications

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“…Bacterial Hsps may play an important role in inflammation (71), and human Hsp60 and H. pylori HspB have antigenic similarities (31). An Hsp60 epitope is detected on the surface of both human gastric cancer cells and human gastric biopsy specimens, and the intensity of cell surface Hsp60 correlated significantly with adhesion of H. pylori to human gastric cancer cells (29).…”

Section: Discussionmentioning

confidence: 99%

Anti-CagA Immunoglobulin G Responses Correlate with Interleukin-8 Induction in Human Gastric Mucosal Biopsy Culture

Ando

Pérez-Pérez

Kusugami

et al. 2000

Clin Diagn Lab Immunol

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Helicobacter pylori persists in the human stomach despite eliciting both cellular and humoral immune responses and inducing proinflammatory cytokines. To determine whether local humoral and cytokine responses are related to each other and to histologic responses, we studied 66 Japanese patients who underwent gastroscopy. Using specific enzyme-linked immunosorbent assays, we examined gastric antral mucosal-organ biopsy culture supernatants to assess interleukin-6 (IL-6) and interleukin-8 (IL-8) levels and antibody responses to H. pylori whole-cell antigens CagA, HspA, and HspB. Of the patients studied, 11 were H. pylori negative and 55 were H. pylori positive; by PCR, all strains were cagA ؉ . As expected, compared to H. pylori-negative patients, H. pylori-positive patients had significantly higher humoral responses to all H. pylori antigens and had higher IL-8 (47.8 ؎ 3.5 versus 10.1 ؎ 4.3 ng/mg of biopsy protein; P < 0.001) and IL-6 levels (2.8 ؎ 0.3 versus 0.26 ؎ 0.2 ng/mg of protein; P < 0.001). Among the H. pylori-positive patients, supernatant anti-CagA immunoglobulin G (IgG) levels were significantly associated with H. pylori density (P < 0.005) and neutrophil infiltration (P < 0.005) scores. Anti-CagA immunoglobulin A levels were correlated with intestinal metaplasia (P < 0.05). Mononuclear cell infiltration scores were significantly associated with supernatant IL-6 levels (P < 0.005) and with IgG responses to whole-cell antigens (P < 0.05). Supernatant IL-8 levels were significantly associated with anti-CagA IgG (r ‫؍‬ 0.75, P < 0.001). Anti-CagA responses correlated with neutrophil infiltration, intestinal metaplasia, H. pylori density, and IL-8 levels, suggesting that the absolute levels of these antibodies may be markers for gastric inflammation and premalignant changes in individual hosts.

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Section: Discussionmentioning

confidence: 99%

Anti-CagA Immunoglobulin G Responses Correlate with Interleukin-8 Induction in Human Gastric Mucosal Biopsy Culture

Ando

Pérez-Pérez

Kusugami

et al. 2000

Clin Diagn Lab Immunol

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“…For example, H. pylori-derived HSP60 (Hp-HSP60) is an important antigen that is abundantly expressed under various environmental stressors 113) . Hp-HSP60 has been found to appear on antigen-presenting cells in the germinal center in the gastric lymphoid tissues of patients infected with H. pylori 114) , and antibodies cross-reactive to both endogenous HSP60 and Hp-HSP60 have been found in the sera of H. pyloriinfected patients 115,116) . Notably, IgG antibodies against a particular amino acid sequence of Hp-HSP60 are able to recognize full-sequenced human HSP60, indicating that immune responses against HSP60 of pathogenic origin are misdirected to a human counterpart 117) .…”

Section: H Pylori and Oxidative Stressmentioning

confidence: 99%

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

Yang

Lü

2014

JAT

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Accumulating evidence implicates Helicobacter pylori (H. pylori) infection in the pathogenesis of certain diseases localized outside the stomach, particularly those characterized by persistent and lowgrade systematic inflammation. Recently, the role of H. pylori infection in the development of atherosclerosis and its clinical complications has received attention. Atherosclerosis is a high-cost disease, and acute events resulting from this condition rank first among morbidity and mortality statistics in most industrialized countries. Atherosclerosis is a multifactorial disorder, and traditional risk factors explain only 50% of its etiology. Therefore, identifying new risk factors for atherosclerosis is necessary. Serological studies indicate that chronic H. pylori infection, especially that with more virulent strains, may predispose patients to the onset of atherosclerosis and related adverse clinical events, and PCR studies have detected H. pylori DNA in atherosclerotic plaques, although this finding remains controversial. If this association were to be confirmed, its importance to public health would be substantial, as the eradication of H. pylori is more straightforward and less costly than the longterm treatment of other risk factors. This review investigates the potential relationship between H. pylori infection and atherosclerosis from both epidemiological and pathogenic perspectives and characterizes the potential mechanisms underlying this correlation.

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“…Our previous studies have shown that the 60-kDa hsp (hsp60) is expressed in the follicular dendritic cells of the gastric mucosa in patients with gastric MALT lymphoma (15) and that antibodies to human hsp60 can be detected in MALT lymphoma patients (14). These results indicate that hsp60 may be associated with the host immune reaction in H. pylori infection, specifically, the pathogensis of gastric MALT lymphoma.…”

mentioning

confidence: 82%

“…Diagnosis of the other diseases was determined according to the symptoms and by endoscopy. Infection with H. pylori was confirmed by culture, the rapid urease test, and histology of gastric biopsy specimens and by the presence of serum antibodies to H. pylori as detected by enzyme-linked immunosorbent assay (ELISA) (14). H. pylori was detected in the gastric mucosae of all patients whose sera were positive for anti-H. pylori antibodies.…”

Section: Methodsmentioning

confidence: 99%

“…The results indicate that a long-standing H. pylori infection induced the Th-2 reaction against hsp60 in patients with gastric MALT lymphoma. We have reported that autoimmunity through human hsp60 is involved in patients with MALT lymphoma (14,15) and that it may be caused by a long-term Th-2 reaction against bacterial hsp60. Infection with H. pylori also leads to an IgG response against the bacteria and hsp60 in patients with peptic ulcer and gastritis.…”

Section: Vol 8 2001mentioning

confidence: 99%

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Immunoglobulin G1 Antibody Response toHelicobacter pyloriHeat Shock Protein 60 Is Closely Associated with Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma

Ishii

Yokota

Sugiyama

et al. 2001

Clin Diagn Lab Immunol

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Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is related to Helicobacter pylori infection. Specifically, it has been pointed out that pathogenesis of MALT lymphoma involves the 60-kDa heat shock protein (hsp60). To investigate humoral immune responses to the H. pylori hsp60 in patients with gastroduodenal diseases and patients with MALT lymphoma, the hsp60 of H. pylori was expressed with a glutathione S-transferase fusion protein and was purified (recombinant hsp60). Sera were obtained from H. pylori-positive patients with gastroduodenal diseases (MALT lymphoma, n ‫؍‬ 13; gastric ulcer, n ‫؍‬ 20; duodenal ulcer, n ‫؍‬ 20; gastritis, n ‫؍‬ 20) and from H. pylori-negative healthy volunteers (n ‫؍‬ 9). Sera from patients with MALT lymphoma were also obtained at two times: before and after eradication therapy. Antibodies to hsp60 and H. pylori were assessed by enzyme-linked immunosorbent assay. The levels of immunoglobulin G (IgG) antibodies to the hsp60 of H. pylori-positive patients with gastroduodenal diseases were significantly elevated compared to those in the controls. The levels of IgG1 antibodies to hsp60 were elevated and correlated with the levels of anti-H. pylori antibodies in patients with MALT lymphoma. Humarol immunity against hsp60 may be important and relevant to gastroduodenal diseases induced by H. pylori infection.Helicobacter pylori is now recognized as a cause of gastritis, peptic ulcer, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma (9, 19). Several H. pylori pathogenic factors, including CagA and VacA, may contribute to the gastric mucosal damage (6, 7). In recent years, it has also been accepted that host immune reactions play an important role in the pathogenesis of H. pylori infection. Although H. pylori is a noninvasive bacterium and is restricted to gastric epithelial cells, infection with H. pylori induces humoral and cellular immune responses in the gastric mucosa (16,22). Bacterial attachment causes induction of interleukin-8 (IL-8) release, and Cag proteins evoke activation of nuclear factor-B and release of IL-8 that may support leukocyte attachment during inflammation (8,17,21). However, the bacterial antigens associated with inflammation are still not clear.Heat shock proteins (hsp's) are immunodominant antigens in various diseases including H. pylori infection (4, 26). Our previous studies have shown that the 60-kDa hsp (hsp60) is expressed in the follicular dendritic cells of the gastric mucosa in patients with gastric MALT lymphoma (15) and that antibodies to human hsp60 can be detected in MALT lymphoma patients (14). These results indicate that hsp60 may be associated with the host immune reaction in H. pylori infection, specifically, the pathogensis of gastric MALT lymphoma.In the present study, H. pylori hsp60 recombinant protein was expressed, and the levels of immunoglobulin G (IgG), IgG1, IgG2, IgM, and IgA antibodies to hsp60 in sera were measured in patients with gastric ulcer, duodenal ulcer, gastritis, and gastric MALT lympho...

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Antibodies to human gastric epithelial cells and heat shock protein 60 in Helicobacter pylori positive mucosa associated lymphoid tissue lymphoma

Cited by 48 publications

References 17 publications

Anti-CagA Immunoglobulin G Responses Correlate with Interleukin-8 Induction in Human Gastric Mucosal Biopsy Culture

Anti-CagA Immunoglobulin G Responses Correlate with Interleukin-8 Induction in Human Gastric Mucosal Biopsy Culture

Helicobacter pylori—An Infectious Risk Factor for Atherosclerosis?

Immunoglobulin G1 Antibody Response toHelicobacter pyloriHeat Shock Protein 60 Is Closely Associated with Low-Grade Gastric Mucosa-Associated Lymphoid Tissue Lymphoma

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