Abstract
Helicobacter pylori causes persistent infection in the gastric epithelium of more than half of the world’s population, leading to the development of severe complications such as peptic ulcer diseases, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. Several virulence factors, including cytotoxin-associated gene A (CagA), which is translocated into the gastric epithelium via the type 4 secretory system (T4SS), have been indicated to play a vital role in disease development. Although infection with strains harboring the East Asian type of CagA possessing the EPIYA-A, -B, and -D sequences has been found to potentiate cell proliferation and disease pathogenicity, the exact mechanism of CagA involvement in disease severity still remains to be elucidated. Therefore, we discuss the possible role of CagA in gastric pathogenicity.
Highlights
Helicobacter pylori is the most common bacterium, which colonizes the gastric epithelium of more than 50% of the world’s population [1,2]
Once H. pylori is transmitted to the gastric lumen, a permanent infection is established in the stomach, and if left untreated, leads to several gastro-duodenal conditions such as chronic gastritis, gastric ulcer, duodenal ulcer, gastric cancer, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma [8,9]
We reported the dominant presence of asparagine (N), serine (S), valine (V), and serine (S) at cytotoxin-associated gene A (CagA) site 314, 594, 684, and 1077, respectively, in strains isolated from gastric cancer when compared with the presence of amino acids in strain 26695, whereas serine (S), leucine (L), valine (V), and threonine (T) were in the majority of strains isolated from MALT lymphoma patients [36]
Summary
Helicobacter pylori is the most common bacterium, which colonizes the gastric epithelium of more than 50% of the world’s population [1,2]. The development of severe gastric complications, such as chronic gastritis, peptic ulcer diseases, and gastric cancer, has been associated with infection with strains expressing the intact cagPAI [13,22]. In a recent study conducted in 263 patients in Alaska, the presence of intact cagPAI was detected in 150 (57%) of H. pylori strains that were found to be associated with the development of more severe gastric pathology. We reported the dominant presence of asparagine (N), serine (S), valine (V), and serine (S) at CagA site 314, 594, 684, and 1077, respectively, in strains isolated from gastric cancer when compared with the presence of amino acids in strain 26695, whereas serine (S), leucine (L), valine (V), and threonine (T) were in the majority of strains isolated from MALT lymphoma patients [36]
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