Journal of Gastroenterology and Digestive Diseases

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (629)348-3199

Mini Review - Journal of Gastroenterology and Digestive Diseases (2023) Volume 8, Issue 1

Autoimmune illness and chronic gastritis caused by helicobacter enteric bacteria.

Aimi Jhon*

Department of Public Health, Kyushu University School of Medicine, Fukuoka, Japan

*Corresponding Author:
Aimi Jhon
Department of Public Health
Kyushu University School of Medicine
Fukuoka, Japan

Received: 29-Jun-2022, Manuscript No. JGDD-22-72928; Editor assigned: 01-Jul-2022, PreQC No. JGDD-22-72928(PQ); Reviewed: 15-Jul-2022, QC No. JGDD-22-72928; Revised: 19-Jul-2022, Manuscript No. JGDD-22-72928(R); Published: 26-Jul-2022, DOI:10.35841/jgdd-7.7.134

Citation: Jhon A. Autoimmune illness and chronic gastritis caused by helicobacter enteric bacteria. J Gastroenterology Dig Dis. 2022;7(7):134

Visit for more related articles at Journal of Gastroenterology and Digestive Diseases


In the human stomach, Helicobacter pylori have developed a particularly peculiar ecological niche. In vitro H. pylori can survive at a pH of 4, and urease activity is necessary for the bacterium to infiltrate animals. In a pH range between 4 and 7, urease does not, however, significantly contribute to the organism's ability to survive. Preliminary research suggests that new proteins are produced when H. pylori cells are brought down from pH 7 to pH 3, and the gene encoding a P-type adenosine triphosphatase that may catalyse NH4+/H+ exchange across the cytoplasmic membrane has been cloned. Other mechanisms of pH homeostasis are still poorly understood.


DGGE, DNAsequencing, Helicobacter, Liver cancer.


The gram-negative, microaerophilic, spiral (helical), Helicobacter pylori, formerly known as Campylobacter pylori, is typically located in the stomach. Its helical structure is assumed to have evolved to allow it to pierce the mucoid lining of the stomach and spread infection. This shape gives rise to the genus name "helicobacter." The Australian doctors Barry Marshall and Robin Warren were the ones to discover the bacterium for the first time in 1982. H. pylori has been linked to lymphoid tissue in the stomach as well as cancer of the mucosa-associated lymphoid tissue in the oesophagus, colon, rectum, or tissues around the eyes, which is known as extranodal marginal zone B-cell lymphoma of the cited organ (termed diffuse large B-cell lymphoma) [1].

Although H. pylori infection typically causes no symptoms, it can occasionally result in stomach ulcers or gastritis. Stomach or first segment of small intestine ulcers. Additionally, the infection has been linked to the emergence of several malignancies. Many researchers have hypothesised that H. pylori influences or protects against a variety of different disorders, but many of these connections are still debatable [2].

Over 50% of the world's population was thought to have H. pylori in their upper gastrointestinal tracts in 2015, with developing nations having the highest prevalence of this illness. However, the frequency of H. pylori colonisation of the gastrointestinal tract has decreased in many nations over the past few decades [3].

Signs and Symptoms

Up to 90% of those with H. pylori infections never show any signs of illness or problems. H. pylori infection, however, increases a person's lifetime risk of getting peptic ulcers by 10% to 20%. Acute infection can manifest as acute gastritis with nausea or stomach pain. When chronic gastritis results, the symptoms, if any, are frequently those of nonulcer dyspepsia, including stomach aches, nausea, bloating, belching, and occasionally vomiting. Pain can happen at other times; however it usually happens when the stomach is empty, in between meals, and in the early morning. The less frequent ulcer symptoms are nausea, vomiting, and appetite loss [4].

Black stools are a sign of gastrointestinal bleeding, which can also happen. Prolonged bleeding can cause anaemia, which makes you feel weak and exhausted. Hematemesis, hematochezia, or melena may happen if there is significant bleeding. Duodenal ulcers are more likely to develop from inflammation of the pyloric antrum, which joins the stomach and duodenum, whereas gastric ulcers are more likely to develop from inflammation of the corpus, or stomach's body. H. pylori infection can cause gastric or colorectal polyps, which are benign growths of tissue that protrude from the mucous membranes of these organs. Although these polyps are typically asymptomatic, dyspepsia, heartburn, upper gastrointestinal haemorrhage, and, occasionally, gastric outlet obstruction may be caused by gastric polyps.

People who have a persistent H. pylori infection are more likely to develop a malignancy that is directly linked to this infection. These malignancies include stomach adenocarcinoma, diffuse large B-cell lymphoma of the stomach, extranodal marginal zone B-cell lymphomas of the stomach, and, less frequently, adenexa of the eye (i.e., orbit, conjunctiva, and/or eyelids), colon, rectum, or oesophagus. The cited linkages include information on the pathogenesis, symptoms, signs, and diagnosis of various malignancies [5].


Signs and symptoms

Morphology: Helicobacter pylori is a Gram-negative, helixshaped bacterium that is around 3 m in length and 0.5 m in diameter. It is not a spirochaete. Gram stain, Giemsa stain, haematoxylin-eosin stain, Warthin-Starry silver stain, acridine orange stain, and phase-contrast microscopy can all be used to show H. pylori in tissue. It can change from spiral to a potentially viable but nonculturable coccoid form and it can also produce biofilms.

Since all gastric and enterohepatic Helicobacter species have flagella, Helicobacter pylori possesses four to six flagella at the same place. Two copolymerized flagellins, Fla A and Fla B, make up the distinctive sheathed flagellar filaments of Helicobacter.


Numerous different strains of Helicobacter pylori exist, and hundreds of them have had their entire genomes sequenced. The "26695" strain's genome has 1,576 genes and a total of 1.7 million base pairs. The aggregate set of 30 sequenced strains, known as the pan-genome, codes for 2,239 different protein families. 1,248 of these, or the universal core, are conserved across all 30 strains. The remaining 991 are the accessory genome, which contains 277 unique OGs that are found in just one strain.


The results of this study suggest that, in Mexico City, water used for human consumption and irrigation may play an important role as a vehicle in the transmission of H. pylori as well as infection by other known enteric pathogens.


  1. Mazari-Hiriart M, Lopez-Vidal Y, Castillo-Rojas G, et al. Helicobacter pylori and other enteric bacteria in freshwater environments in Mexico City. Arch Med Res. 2001;32(5):458-67.
  2. Indexed at, Google Scholar, Cross Ref

  3. McGowan CC, Cover TL, Blaser MJ. Helicobacter pylori and gastric acid: biological and therapeutic implications. Gastroenterol. 1996;110(3):926-38.
  4. Indexed at, Google Scholar, Cross Ref

  5. Cave DR. How is Helicobacter pylori transmitted?. Gastroenterol. 1997;113(6):S9-14.
  6. Google Scholar, Cross Ref

  7. Sibony M, Jones NL. Recent advances in Helicobacter pylori pathogenesis. Curr Opin Gastroenterol. 2012;28(1):30-5.
  8. Indexed at, Google Scholar

  9. Bode G, Mauch F, Malfertheiner P. The coccoid forms of Helicobacter pylori. Criteria for their viability. Epidemiol Infect. 1993;111(3):483-90.
  10. Indexed at, Google Scholar, Cross Ref

Get the App