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Author Spotlight: Gastric Epithelial Cell Responses in Helicobacter pylori infection
Published on: July 5, 2024
Regulatory B cells (Bregs) in Helicobacter pylori chronic infection
Noha A Hassuna1, Sahar Sh Hussien1, Mohammed Abdelhakeem2
1Medical Microbiology and Immunology Department, Faculty of Medicine, Minia University, Minia, Egypt.
Background:
Helicobacter pylori (H. pylori) infection is linked with a wide variety of diseases and was reported in more than half of the world's population. Chronic H. pylori infection and its final clinical outcome depend mainly on the bacterial virulence factors and its ability to manipulate and adapt to human immune responses. Bregs blood levels have been correlated with increased bacterial load and infection chronicity, especially Gram-negative bacterial infection. This study aimed to identify prevalence and virulence factors of chronic H. pylori infection among symptomatic Egyptian patients and to examine its possible correlation to levels of regulatory B cells (Bregs) in blood.
Materials And Methods:
Gastric biopsies and blood samples from each of 113 adult patients, who underwent upper endoscopy, were examined for the detection of H. pylori by culture and PCR methods. Conventional PCR was used to determine various virulent genes prevalence and association to clinical outcome. Flow cytometry was used to evaluate Bregs levels.
Results:
Helicobacter pylori prevalence was 49.1% (55/112). Regarding virulence genes incidence, flaA gene was detected in 73% (40/55), vir B11 in 56.4% (31/55), hopZ1 in 34.5% (19/55), hopZ2 in 89% (49/55), babA2 in 52.7% (29/55), dupA jhp917 in 61.8% (34/55), vacA m1/m2 in 70.9% (39/55), and vacA s1/s2 in 69% (38/55) strains. Bregs levels were significantly lower in H. pylori-infected patients (p = 0.013), while total leukocyte count (TLC) showed no significant differences.
Conclusion:
Helicobacter pylori infection prevalence was almost 49%, and the infection was found to be related to inflammatory conditions as gastritis and ulcers rather than malignant transformations. Also, we found that CD24+ CD38+ B cells were downregulated in H. pylori-infected patients.
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