Can You Get H Pylori Again if You Have Already Had It
Malays J Med Sci. 2022 Sep; 22(v): lxx–75.
Why practise nosotros still take Helicobacter Pylori in our Stomachs
Amin Talebi Bezmin Abadi
oneDepartment of Bacteriology, Faculty of Medical Sciences, Tarbiat Modares University, PO Box 14115-111, Tehran, Iran
Enzo Ierardi
2Division of Gastroenterology, Department of Emergency and Organ Transplantation, Piazza Giulio Cesare, 70124 Bari, Italy
Yeong Yeh Lee
iiiSchool of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia
Received 2022 Feb 23; Accepted 2022 Jun 17.
Abstruse
The existence of any infectious agent in a highly acidic human stomach is contentious, only the run a risk finding of Helicobacter pylori is by no means an accident. One time H. pylori colonises the gastric mucosa, information technology tin persist for a lifetime, and information technology is intriguing why our immune system is able to tolerate its beingness. Some conditions favour the persistence of H. pylori in the stomach, but other weather condition oppose the colonisation of this bacterium. Populations with loftier and extremely low prevalence of H. pylori provide useful insights on the clinical outcomes that are associated with this type of infection. Adverse clinical outcomes including peptic ulcer illness and gastric cancer depend on a frail remainder between a harmless inflammation and a more severe kind of inflammation. Is the simply good H. pylori really a dead H. pylori? The jury is still out.
Keywords: Helicobacter pylori, survival, elimination, gastric cancer, peptic ulcer disease, stomach
Introduction
In 1893, a spiral course of bacteria was first reported in the gastric mucosa of dogs by the well-known Italian anatomist, Bizzozero(1). However, the very being of any infectious agents in the human tummy was contentious at that time considering of the strong acidic environs of the stomach. The rest was history when Warren and Marshall plant Helicobacter pylori (H. pylori) in antral biopsies of the homo stomach and discovered that this bacterium is the cause of peptic ulcer disease (2). The primary colonisation of H. pylori usually occurs during early childhood and decreases with age, just post-obit an episode of acute gastritis, the infection can last a lifetime (3). Although other microorganisms reside in the man stomach, but H. pylori tin can survive over long periods of fourth dimension. However, the reason for this persistent colonisation is unknown.
What favours the in vitro and in vivo colonization of H. pylori in a hostile gastric environs?
H. pylori tin penetrate deep into the gastric mucosal layer with its ii to 6 polar flagella and also through the product of urease (four), which allows it to meet a more friendly (pH ~ 5–vi) surroundings. The ammonia produced from urea hydrolysis and then acts as a receptor for H+ ions and generates a neutral pH in the intracellular environment. Members of the H. pylori outer membrane proteins (HOP) family of outer membrane proteins marshal with other H. pylori adhesion proteins and assist in the successful bounden of the bacterium to the gastric epithelium (tissue tropism) (v). Bacterial phase variation by gene conversions and slipped strand mispairings enable H. pylori to form new subpopulations and adopt properties that allow for the neutralisation of constructive human immune responses. In add-on, a diverseness of virulence factors including babA2, horB, homB, iceA2, cagA, and dupA ensure that H. pylori persists in humans (six). Although not all of the functions of these factors are completely understood, bachelor data have shown that these genes, virtually of which are pro-inflammatory, have the capacity to change the physiology and morphology of gastric epithelial cells (7,eight).
In most instances, H. pylori causes just minimal damage to the gastric epithelium, and the inflammation is hands kickoff or even ignored by the immune system. Balmy inflammation in the gastric mucosa is associated with two major benefits for H. pylori: kickoff, information technology allows for a more effective harvest of nutrients to feed the leaner, and second, it diminishes any active invasion of immune cells. The almost invincible human immune system fails to eliminate H. pylori because of successful immune evasion strategies and besides considering of the complex intrinsic genetic variability adopted by this bacterium. The immune evasion mechanisms include the following: i) a change in the modulation of the normal function of polymorphonuclear leukocytes (PMNs) and macrophages, ii) an inhibition of lymphocyte proliferation, and iii) a downwards-regulation of some types of surface antigen ligands. To date, non enough evidence has accumulated to betoken an actual cellular invasion by H. pylori, only a most recent report has demonstrated an association between jail cell invasion by this bacterium and gastroduodenal diseases (9). If confirmed, the intracellular presence due to the penetration of the H. pylori bacterium may explain why we yet have a persistent infection of H. pylori in our stomachs.
A number of genetic polymorphisms seem to correlate with an increased risk of gastroduodenal disorders in the infected host (10). For instance, a relatively high expression of sure IL-1β polymorphisms in infected humans has been shown to increase the risk of gastric atrophy and gastric adenocarcinoma. In vitro studies have too revealed a significant link between the expression of TNF-α and aberrant β-catenin signalling and gastric adenocarcinoma. In addition, polymorphisms in IL-10 are associated with severe gastric diseases including gastric cancer in H. pylori-positive individuals. Even among populations with an extremely low prevalence of H. pylori, genetic variations in the UFM1, THBS4, CYP2C19 and MGST1 genes are associated with atrophic gastritis, complete intestinal metaplasia, incomplete metaplasia and dysplasia, respectively (11). These genetic polymorphisms are besides the reasons why H. pylori persists in susceptible hosts, but the verbal functions of these genetic variations are non yet entirely clear. Epigenetic mechanisms may play a office as well. For instance, the epigenetic silencing of FOXD3 by H. pylori has been shown to be an early upshot in gastric carcinogenesis (12).
What Opposes the Persistence of H. pylori Infection?
Antibiotics are major obstacles to the survival H. pylori in the man stomach (13). Available eradication regimes are highly constructive against H. pylori although sporadic reports of resistance to metronidazole and clarithromycin have been published. More recently, it has been shown that H. pylori tin can potentially evade the lethal furnishings of antibiotics through indicate mutations in sure genes (xiv) (east.k., rdxA, 16s rRNA, 23s rRNA and gyrA).
Probiotics, especially Lactobacilli, may play a role in the inhibition of H. pylori colonization (15) because some studies have reported an inverse correlation between the colonisation of H. pylori and the density of Lactobacilli in the human stomach. Furthermore, certain foods with antimicrobial backdrop may be the reason for the observed low prevalence of H. pylori infection in certain populations such as the Malays (16).
It is known that the distribution of H. pylori is not homogeneous within the stomach and that this may be a result of constant and strong peristaltic movement (17). It is also possible that peristalsis inside the stomach acts as a deterrent to the survival of H. pylori.
The expression of protective genes in the host may explain the low prevalence of H. pylori infection in certain populations. For example, in the Malays vs the Chinese or the Indians, genetic polymorphisms in the C7orf10, TSTD2, SMG7, and XPA genes were institute to be significantly associated with an absence of H. pylori infection (18). Although the verbal functional roles of these polymorphisms remain to be determined, these genes may code for enzymes that are involved in the metabolism of compounds that inhibit the survival of H. pylori, and they may also lawmaking for proteins that let for the repair of aberrant genomes.
Lessons from Populations with a High and Depression Prevalence of H. pylori Infection
Populations with a high prevalence of H. pylori infection (above 60%) such as Cathay, Nippon, and Korea also take a loftier incidence of H. pylori-associated diseases including gastritis and gastric adenocarcinoma. However, these diseases practice non occur solely as a result of H. pylori, but ofttimes, other associated environmental factors including poor sanitation and hygiene promote the transmission of the bacterium. Moreover, the concomitant utilize of aspirin, non-steroidal anti-inflammatory drugs (NSAIDs) and or traditional preparations that contain steroids tin hurt the epithelium of the tummy (nineteen). As described in the above sections, bacterial factors would as well be important in the perpetuation of infection and of H. pylori-associated diseases(20). It is unclear, withal, why the rate of gastric cancer is depression among Indians and Africans despite the high prevalence of H. pylori in these populations (Asian enigma). Again, environmental, genetic and bacterial factors may be of import (21). For example, in the Indian province of Kashmir, the reported charge per unit of gastric cancer is three–6 times higher than that in other districts including Bangalore, Madras and Bombay. The high consumption of salt and preserved foods in the Kashmir population compared with the consumption of fresh fruits and vegetables by Indians in the southern districts may explain the inverse relationship betwixt the presence of H. pylori and gastric cancer. Populations with a low prevalence of H. pylori infection including Malays in South-Due east Asia also have a depression incidence of H. pylori-associated diseases (22). Environmental factors including consumption of foods with inhibitory activities against H. pylori also as protective genetic factors may exist the reasons for the depression prevalence of infection and diseases (22). Moreover, the diverse virulence factors in H. pylori are important bacterial factors that can influence clinical outcomes. Mixed virulence genotypes, specially the less virulent types in Malays, may have provided them with protection against H. pylori-associated diseases (23).
Volition H. pylori Continue to Infect our Stomachs? A Verdict
Figure ane summarises the forces that favour and oppose the survival of H. pylori. The balance seems to favour the persistence of H. pylori, but lessons from populations with a low prevalence of infection suggest that humans are probably amend without H. pylori than for the bacterium to persist in the tummy. Is the only expert H. pylori a dead H. pylori? No one really knows the respond. More than half of the world's population harbours H. pylori, but merely a minority of individuals subsequently develop severe forms of gastric diseases, specially gastric adenocarcinoma and peptic ulcer affliction.
Weather condition or forces that favor survival or elimination of H. pylori in the human stomach.
Without the symbiotic or commensal relationship with human hosts that has developed over thousands of years, it may have been hard for H. pylori to persist. The maintenance of a frail balance betwixt a harmless inflammation and a more severe grade of inflammation seems to exist the determining factor for adverse clinical outcomes (Figure ii). The imbalance in this relationship probably occurs considering the man host becomes weak at some point, which allows the bacterium to become stronger (more inflammation and therefore more severe disease) and vice versa. In reality, if Darwin could have his style, the stronger survivor will win.
Increasing severity of digestive diseases in the case of imbalanced relationship between H. pylori and the human being host.
Footnotes
Funds
None.
Conflicts of Involvement
None.
Authors' Contributions
Formulation and pattern, analysis and interpretation of the data, drafting of the article, disquisitional revision of the article for the of import intellectual content, last approval of the commodity, provision of written report materials or patient, statistical expertise, obtaining of funding, authoritative, technical or logistic support and collection and assembly of information: ATBA, EI, YYL
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