International Research Journal of Microbiology

Abstract

Communities of microorganisms attached to a surface are bacterial biofilms. The formation of biofilms is necessary for both infection success and environmental survival. Helicobacter pylori are one of the most well-known reasons for bacterial disease in people. A few examinations showed that this microorganism has biofilm framing capacity in the climate and on human gastric mucosa epithelium as well as on in vitro abiotic surfaces. In the climate, H. pylori could be implanted in drinking water biofilms through water circulation framework in created and emerging nations so the drinking water might act as a repository for H. pylori contamination. One possible explanation for the failure of eradication therapy is the formation of biofilms by H. pylori on the surface of the gastric mucosa in the human stomach. Finally, H. pylori biofilm formation can reduce antibiotic susceptibility, according to in vitro studies, and H. pylori antibiotic resistance mutations are more prevalent in biofilms than in planktonic cells. Based on these findings, biofilm formation by H. pylori may be an important factor in controlling and preventing H. pylori infections. Accordingly, examination of H. pylori biofilm development could be compelling in explaining the itemized systems of contamination and colonization by this microorganism.

Keywords

Bacterial biofilm, Environmental survival, Gastric mucosa, Microorganism, Antibiotic resistance

INTRODUCTION

Helicobacter pylori are a winding, microaerophilic, painless, gram negative bacterium that colonizes the human gastrointestinal lot, essentially the stomach. One of the most common causes of human infection is H. pylori, especially in developing nations where up to 90% of the population can be infected. H. pylori disease frequently endures all through life. This creature has been distinguished as an etiological specialist of ongoing dynamic gastritis, peptic ulcer illness, gastric adenocarcinoma, and Mucosa Related Lymphoid Tissue (MALT) lymphoma. In addition, the World Health Organization's International Agency for Research on Cancer's working group came to the conclusion in 1994 that H. pylori are a group I known human carcinogen. Even though most people infected with H. pylori don't show any symptoms, infected people are at high risk for the diseases listed above. Various factors, for example, the vacuolating cytotoxin, the cagA and cag Pathogenicity Island (cagPAI), motility, adhesins, and the urease protein are known to be engaged with the harmfulness of this creature. There are two morphological variations of H. pylori. One is a winding structure and the other is a non culturable yet suitable coccoid structure. The twisting structure is the most wellknown structure associated with colonization of the human stomach. Some recent studies have suggested that H. pylori can grow biofilms in vitro. H. pylori can also form biofilms on the mucosa of the stomach. Additionally, H. pylori could be implanted in drinking water biofilms on the surfaces of water circulation frameworks increated and agricultural nations (Marshall J, 1984).

Development of bacterial biofilm

The majority of bacteria survive in severely depleted environments. Bacteria frequently form surface-attached communities known as "bacterial biofilms" in order to shield themselves from harmful environmental influences. Numerous chronic infections have been linked to biofilms, which are common in clinical, industrial, and natural settings. Typically, biofilms are made up of multiple bacterial species. More than 500 distinct bacterial species, for instance, can be found in dental biofilms, also known as dental plaque. Biofilms are made up of dead and alive microbial cells as well as a wide variety of self-generated extracellular polymeric substances (EPS) like proteins, nucleic acids, and polysaccharides. The biofilm biomass can make up up to 90% of the EPS matrix. The underlying connection is driven by hydrophobic or electrostatic collaborations too as unambiguous bacterial surface atoms. The next step is for the bacteria to multiply and create microcolonies with EPS surrounding them. With increasing numbers of bacteria, the biofilm forms thick, tower-like or mushroom-like structures in the third step (maturation step). Thusly, the augmented biofilm shows central disintegration furthermore, frees planktonic bacterial cells which can spread to different areas (Dunn BE, 1997).

In comparison to planktonic cells, biofilm bacteria have distinct characteristics. One of these is an expanded protection from antimicrobial specialists. It has been demonstrated that biofilm cells are less susceptible to antimicrobial agents than planktonic cultures, which is a significant factor in the etiology of infectious diseases. The fact that biofilm cells displayed a distinct pattern of gene expression, including the expression of virulence factor genes, is yet another distinctive feature. Quorum Sensing (QS), a cell-to-cell communication system, may be involved in this property. The flagging atoms are known as Auto Inducers (AIs). At the point when these particles come to a basic edge fixation, a sign transduction overflow is triggered. Announcing AIs in the QS framework shapes the reason for changes in different quality articulations including destructiveness factors, discharge framework, motility, sporulation, and biofilm development (Blaser MJ, 1992).

Characterization of H. pylori biofilm

Biofilms on glass surfaces were formed by H. pylori strains used in their study, including clinical isolates, laboratory strains, and a mouse-adapted strain. Also, they said that H. pylori could only form a biofilm at the air-liquid interface, which probably means that it is micro aerobatic. However, H. pylori biofilm formation has not been extensively studied at this time. As a result, we investigated the underlying mechanisms behind H. pylori strains' capacity to form biofilms. At first, we laid out a plausible and stable model for biofilm development by this microorganism. Momentarily, sanitized glass coverslips were put into 12-well micro titer plates. Each very much was loaded up with 2 mL of Brucella stock enhanced with 7% Fetal Calf Serum (FCS)to permit adherence of H. pylori at the air-fluid point of interaction. The development of biofilms was started by immunizing approximately 5 × 105 cells into each well. For three to five days, the cultures were incubated with shaking in micro aerobic conditions at 37°C. Eight H. pylori strains, including standard SS1, ATCC 43579, ATCC 43579, and NCTC11638 strains, as well as clinical isolates from Japanese patients, were examined using this model (Graham DY, 1989).

At the liquid-gas interface of the cultures, all of the strains developed biofilms under these conditions. In particular, biofilm formation was significantly higher in strain TK1402, which was isolated from a Japanese patient with duodenal and gastric ulcers. The relative thickness of the biofilms showed that TK1402 had a strong ability to form biofilms. Concerning the H. pylori biofilm framework, demonstrated that extracellular DNA plays a crucial role in the stabilization of biofilm structures and is a component of EPS structures. Proteomannans, or mannose-related proteoglycans, are one of the EPS structures and that proteomannans are also involved in the formation of H. pylori biofilms. They also reported that biofilm formation with a napA-deficient mutant exhibited a distinct phenotypic biofilm and that the Neutrophil-Activating Protein A (NapA) is upregulated in biofilm cells in comparison to planktonic cells. In the biofilms made by multiple H. pylori strains are more complex than those made by one strain, and that these conditions may encourage genetic exchange, which favors the creation of more virulent strains (Parsonnet J, 1991).

Biofilm forming environment

The sequenced H. pylori genome contains only one known quorum-sensing gene, the luxS gene. According to a number of studies, H. pylori produces extracellular signaling molecules that are associated with AI-2, and the production of AI-2 depends on how well luxS functions. According to these reports, luxS production of AI-2 is correlated with growth phase, with peak production occurring during the middle of the exponential growth phase. According to a number of studies, LuxS plays a different role in regulating motility by influencing flagellar biosynthesis and transcription (Wotherspoon AC, 1993).

Environmental biofilm formation

For H. pylori, contact between people via the faecaloral, oral-oral, or gastro-oral routes is thought to be the most common method of transmission. However, the patterns of H. pylori transmission suggest a universal source of exposure rather than person-to-person transmission, particularly in developing nations. As a result, the drinking water supply was identified as a significant source of H. pylori infection, and in fact, H. pylori were only detected by special methods in water distribution systems. Also, the job of water sources and related biofilms going about as environmental transmitters of H. pylori has been recommended by the recognition of H. pylori DNA by atomic strategies, for example, PCR, in sewage, well water, lake and stream water, stream water, also, shallow ground water in created nations as well as in agricultural nations . These findings suggested that H. pylori is present in water distribution systems and may thrive there in biofilms. However, it does not appear that H. pylori forms biofilms in areas with relatively stressful conditions like low temperatures and a lack of nutrients. The bacterial genera Pedomicrobium, Hyphomicrobium, Gallionella, and Caulobacter were frequently observed in oligotrophic water systems (Liu D, 2023). Gastric mucosal biofilm formation The first photographic evidence of the presence of H. pylori biofilms on human gastric mucosa. Utilizing scanning electron microscopy and endoscopically directed biopsies. H. pylori positive samples had mature biofilms attached to the cell surface. Their gathering thusly detailed that, among patients with peptic ulcer illness who were tried urease positive for H. pylori, the typical pace of all out cell surfaces covered by biofilms was 97.3%, instead of 1.64% for urease negative patients . A pervasive S-shape H. pylori morphotype which existed together with coccid accumulated microbes implanted in a plentiful network was shown by SEM examination with biopsies from patients holding onto culturable microbes. However, samples from patients who were only identified as H. pylori positive using molecular methods revealed clusters of coccid bacteria arranged in a microbial biofilm. SEM analysis of gastric biopsies revealed that H. pylori formed biofilms on the gastric mucosa in all patients who had a history of at least four H. pylori eradication failures and that the biofilm disappeared in all patients when the microorganism was eradicated (Bijlsma JJE, 1999).

Therapy for preventing H. pylori infection

Antitoxin obstruction in H. pylori can accordingly be procured by the choice of unconstrained change occasions that happen because of the extent and span of antimicrobial use on the human gastric mucosa. Nakamura and team reported that CAM concentrations in gastric juices, mucosa, or serum were 550.6, 64.6, and 2.5 g/mL at 2 hours and 43.4, 36.2, and 2.2 g/mL at 6 hours, respectively, after administration of 500 mg of the drug for 7 days (Bode G, 1993). These concentrations may be adequate to decrease the degrees of H. pylori in vivo so this microorganism framed biofilms. However, the medication must be taken in a sufficient amount for such high concentrations to remain on the gastric mucosa for an extended period of time. Additionally, the gastric mucosal concentration of CAM does not reach high levels in cases of inadequate compliance with eradication therapy. In addition, pediatric, respiratory, and otorhinolaryngology settings frequently utilize macrolides, including CAM, for the treatment of various infectious diseases. H. pylori's formation of biofilms may play a role in developing CAM resistance in these instances. Novel ways to deal with forestall biofilm arrangement and to treat diseases by biofilm-framing microorganisms are presently being worked on (Cellini L, 1994).

CONCLUSION

Within biofilms, pathogenic bacteria like H. pylori can evade both the immune responses of the host and the effects of antibiotics. As a result, biofilm forming bacterial infections that persist become problematic and challenging to treat. H. pylorus has been shown to form biofilm on human gastric mucosa in some previous research. In any case, appraisal of H. pylori strain helplessness to anti-toxins in vitro has customarily been assessed utilizing planktonic cells, so MICs are not dependable indicators of the anti-toxin impacts in the human stomach. The evaluation of H. pylori's capacity to form biofilms may contribute significantly to the control and prevention of antibiotic resistance. It is normal that improving our insight into H. pylori biofilm arrangement will prompt new treatment treatments for forestalling H. pylori diseases. However, it is acknowledged that our comprehension of the formation of biofilms by H. pylori is still in its infancy. The mechanism of H. pylori biofilm formation requires additional research. Additionally, if conventional antibiotics, biofilm dissolving compounds, and quorum sensing inhibitors are investigated as novel H. pylori eradication strategies for the human gastric mucosa, they may offer advantages in eliminating H. pylori infections.