What about the early years of J. Robin Warren? There have been several reports describing the presence of spiral bacteria in the stomach over the past 100 years, but they have not been taken seriously. For example, in 1940 Freedburg found a few cases and made a short report. However, a special study conducted by Palmer in 1954 denied the existence of such bacteria in the stomach. The dogma of medical textbooks is also clear enough that no bacteria grow in the normal stomach, and that the acid environment in the stomach will kill swallowed microorganisms quickly, and that only microorganisms grow in the atrophied stomach and in the necrotic debris of ulcers, which may be secondary to infection and are mostly fungal. Before the 1970s, it was difficult to obtain high-quality gastric biopsy specimens. Most gastric specimens came from surgery, or even autopsy, and the mucosa of such specimens was mostly autolysed, making it difficult to see fine mucosal pathological changes, and if bacteria were present, they had long since disappeared. At that time, chronic gastritis was rarely seen in pathological examinations, and chronic gastritis was obviously not related to ulcers and gastric cancer. The classification scheme for gastritis at that time had little clinical application except for pernicious anemia related atrophic gastritis and some acute gastritis. Pernicious anemia was a mandatory subject in school, but it was rare in the clinic. The pathology of many biopsy specimens showing chronic gastritis with varying degrees of focal atrophy was not recognized as having any clinical importance. For me, this all suddenly changed after the 1970s. The advent of fiberoptic endoscopy made rapidly well-fixed gastrointestinal mucosal biopsy specimens one of the most commonly seen pathological biopsies. Pathologic studies based on such specimens led to Richard Whiehead’s classification of gastritis in 1972.Whiehead’s classification is complex but very logical, describing biopsy pathology in terms of common, easily identifiable and easily quantifiable indicators, such as site, depth, type, severity of inflammation, atrophy of the gastric glands, intestinalization, etc. Whiehead refers to gastritis as “activity,” i.e., the presence of foci of leukocytic infiltration in the mucosal epithelium, is actually seen frequently in gastric mucosal biopsy pathology, but has been overlooked. My feeling is that the Whiehead classification scheme is easy to learn and easy to use, and the results are stable. In April 1979, during routine H-E pathology of a gastric mucosal biopsy specimen, in addition to the lesions of severe active chronic gastritis, I noticed a strange blue line on the mucosal surface, which, when observed after turning to high magnification, was found to be numerous bacilli clinging to the gastric epithelium. I thought this was unusual, so I showed it to my colleagues. But they all said that they could not see it, which made me very annoyed. I then tried Warthin Starry silver staining of the sections, and the bacteria were clearly visible, visible at low magnification, in greater numbers and to a greater extent than expected. I was overjoyed. Electron microscopy of the wax specimen also clearly showed this large number of bacteria, morphologically similar to Campylobacter spp. Now my colleagues were sure of the existence of this bacterium, but the importance was another matter. I continued to examine all new gastric biopsy specimens for this bacterium, but did not really expect to find them. Surprisingly, they were frequently present, although usually not in as large numbers as the first case and often in a focal pattern. I soon discovered that the bacteria were often found in histologically diagnostic specimens of chronic gastritis, particularly what Whiehead refers to as active gastritis, that is, gastritis with neutrophil infiltration, and that they were seen in nearly half of the sinus mucosal specimens. During this period, whenever such bacteria were found, I noted them on the clinicopathology report form. However, I don’t think anyone would consider them to be of any importance. I think this bacterium is very closely related to chronic gastritis. But I got little support from anyone other than my wife. Many people think it’s garbage. It’s no wonder that this finding didn’t fit the medical philosophy of the era, when the normal stomach was considered sterile. The secretion of stomach acid would quickly kill off any bacteria swallowed. Yeast usually grew in the necrotic debris at the base of the ulcer and must have been secondary to the ulcer. The best comment I got was “even if the bacteria are growing there, they are secondary to gastritis”. And for me, this is wrong. The relationship between the bacteria and the inflammation and the unusual characteristics of the bacteria when they are present suggest that the infection is primary. However, trying to prove this is difficult. I think a negative control trial should be designed would be helpful to confirm this idea. I had never been exposed to the clinic and tried to get some help from the clinicians to take specimens that looked normal on gastroscopy, but the physicians disagreed and told me to “clamp specimens only where needed”. Therefore, their biopsy specimens could be taken from any “needed area” of the stomach, that is, to examine the nature of the ulcer or tumor, and they were taken from the edge of the lesion. These specimens are difficult to distinguish between bacteria-related changes and secondary lesions. The physicians never intended the biopsy specimens to look for bacteria, and the idea of sending gastric biopsy specimens for bacterial culture is even more absurd. “If this bacterium really exists, why hasn’t it been reported before?” I don’t know why I had never seen them before, so this was a difficult question to answer. Only later did I find many previous reports of such bacteria, including some fabulous descriptions from 100 years ago, and it was just that no one had studied them further before. Of course, this was an afterthought. Without the support of my physician, I had to look in the pathology archives for wax pieces of gastric biopsy specimens reported as normal to see if these normal gastric mucosa had this bacterium. I didn’t realize how difficult it would be. Most of the specimens reported as normal were mostly from the gastric body with minimal pathological changes, while the accompanying gastric sinus showed active gastritis and bacteria could be seen. I incorrectly assumed that this bacteria only infected the gastric sinuses. The file did not break down the sites of gastric mucosal biopsies, and it was difficult to find cases in which the report indicated the mucosa of the gastric sinus. However, 20 cases were eventually found. Of these 20 cases, one case was found to have bacteria, and in this patient I re-reviewed the pathology and found moderate gastritis, while the other 19 cases without bacteria were indeed normal. The pathology of the case with bacteria was asked to be re-read by the original reporter, and he reviewed it and recognized that it was a mistake and should have been gastritis. At the same time, almost half of the mucosa of the gastric sinus could find bacteria in the clinical specimen, and as long as the mucosa had bacteria, there was chronic gastritis at the same time, and most of them were active gastritis, and many cases were accompanied by different degrees of atrophy and focal intestinalization. The pathologically normal mucosa of the gastric sinus never shows bacteria. In 1981, just as I was about to publish my findings, a young man appeared, Barry Marshall, a registered gastroenterologist at our hospital, and asked for a scientific paper. – “A pathologist is trying to attribute gastritis to a bacterial infection.” Barry Marshall approached me about it and was not interested in my work nor did he believe my arguments. Fortunately, however, he agreed to provide me with a small series of gastric mucosal biopsy specimens. As I requested, the biopsies were taken from the normal-looking mucosa of the gastric sinus, making sure to avoid obvious lesions such as ulcers. Barry Marshall suddenly showed great interest in this bacterium and devoted his life’s work to the study of it. I still don’t understand how he suddenly became interested. Next, we conducted a formalized study of 100 gastroscopy patients. The data collected included clinical symptoms, standardized sinus biopsies for pathological examination and bacterial cultures to analyze the relationship between bacteria, gastritis and clinical symptoms and gastroscopic presentation. Surprisingly, the histological findings of bacteria and their gastritis were almost independent of most clinical symptoms and gastroscopic manifestations. In terms of clinical symptoms, only halitosis and diaphragms were associated with bacteria, regardless of the gastroscopic presentation, and most of these patients who had gastroscopy had epigastric pain. The gastroscopic diagnosis of gastritis does not coincide with the histological diagnosis of gastritis. In terms of bacterial culture, since this bacterium resembled Campylobacter, we cultured it according to the Campylobacter isolation culture method, but did not add antibiotics to the medium as we did for fecal isolation of Campylobacter. At first, the culture always failed, and only a few positive cases were found until Easter. After a thorough examination and analysis of the cause, it was found that the problem might lie in a leaky incubator. After the incubator was repaired, the culture became very reliable from then on. Finally, Barry Marshall summarized the gastroscopy results and we were amazed to find that all duodenal ulcer patients had this bacteria in their stomachs! All of these findings were very interesting, but the clinicians were still not convinced, and in 1983 I published a short report of my work in a journal, followed by a letter from Barry Marshall about our joint findings. Subsequently, Barry Marshall reported our findings at the Brucella Campylobacter Conference, which attracted the attention of Martin Skirro, a leading authority on Campylobacter in the UK. This was a fortunate opportunity. After the conference, we submitted our findings in the form of a paper. However, we did not hear back for several months because the editorial team had not obtained the approval of a single reviewer, which meant that the paper could not be published. Finally, we contacted Martin Skirro. In April 1984, our paper was finally published word-for-word. We continued our research on this bacterium, and the early studies involved three aspects: diagnosis, treatment, and evidence. Many of the tests on the diagnostic side were proposed by Barry Marshall, such as pre-treatment serological tests, breath tests, rapid urease tests (CLOtest), histology, smears, and cultures. In terms of treatment, Barry Marshall tried bismuth and antibiotics. Regarding bismuth, Barry Marshall was inspired by an old edition of Willian Osler’s internal medicine textbook, and it did work. As for evidence, both Barry Marshall and Dr. Arthur Morris of New Zealand used the Koch principle of identifying the causative organism: the same bacteria can be isolated from all patients, and culture of the bacteria can cause the same lesions. Dr. Barry Marshall’s acute gastritis was severe, but he quickly cured himself. Dr. Arthur Morris kept sending me biopsy specimens, which were consistently bacterial and chronic gastritis, and took years to cure. Some of the early study cases showed different clinical types. For example, the NSAI class of drugs can cause duodenal ulcers, but that does not mean that bacteria do not play a role. My wife was one of the early study cases. She had arthritis that required NSAI drugs, and the arthritis cleared up, but she had stomach pain; she stopped taking the NSAI drugs, and the stomach pain cleared up, but the arthritis came back, and so on. I took her to the doctor and Barry Marshall confirmed that there was bacteria, and after killing the bacteria and continuing the NSAI drugs, the stomach pain stopped. And after my wife was cured, she noticed that I had bad breath, and it was surprising that I also had bacteria, but there was no stomach discomfort at all. We also made a study of double-blind, antibacterial treatment of duodenal ulcer. Patients received acid-suppressive therapy plus an antibacterial agent or placebo. It was found that ulcers without antimicrobial treatment recurred quickly, while ulcers with eradicated bacteria rarely recurred. The role of bacteria in histological gastritis was also shown very clearly. After eradication of the bacteria, the active inflammation shown by histology subsided rapidly. Other changes are slow and incomplete, and anatomical abnormalities such as atrophy, chemosis, and fibrosis are rarely altered. If bacteria are present, the gastritis remains unchanged. Since the report of our study, a worldwide research boom has been set in motion. Gastroenterology studies it in relation to digestive diseases, non-gastroenterology studies it in relation to various non-digestive diseases, and various Helicobacter species have been found in the animal world. Public health issues are of great concern, pharmaceutical companies are investing heavily in the development of effective drugs, >journals have emerged, worldwide H. pylori conferences are held regularly, and countless papers on H. pylori research have been published. People often ask me what it means to me personally to be the discoverer of H. pylori. It is difficult for me to answer. However, this discovery has changed my life. I continue to work as a pathology consultant, and much of my research and writing is done after hours.