Gut check: can other microbes or communities phenocopy H. pylori's early gastric pathology?
Gut check: can other microbes or communities phenocopy H. pylori's early gastric pathology?
复制标题
肠道检查：其他微生物或群落是否可以复制H。幽门螺杆菌的早期胃病理
DOI：
10.1136/gutjnl-2021-325749
复制
发表时间：
2022-07
期刊：
影响因子：
24.5
通讯作者：
Brown JW
中科院分区：
文献类型：
--
作者：
Brown JW
胃粘膜每天暴露于数十亿不同的微生物。为了阻止胃定植以及限制潜在病原体通过胃肠道的更远段，胃具有几种广泛活跃的防御机制：酸度，粘液和蛋白水解酶。其他胃外机制也可能起作用：例如，唾液粘蛋白上的糖基化表位如3′-Sulfo-Lewis A与吞咽的细菌共转运，并在胃内pH值下降时与它们结合，1可能阻止细菌结合粘膜。尽管有这些防御措施，但至少有一种细菌，幽门螺杆菌能够在人类胃中定植。该病原体最初侵入胃窦，但也可通过诱导化生性腺体反应扩散至胃体，2其特征为泌酸壁细胞丧失（泌酸萎缩）和化生性腺体变化（即痉挛性表达多肽化生或SPEM）。在一小部分个体中，化生可进展为异型增生和胃腺癌。因此，确定与H。幽门螺杆菌感染在临床上变得重要。3.与泌酸性萎缩相关的酸度的减少或缺乏创造了允许机会性微生物定植的环境。虽然这些异位微生物群落的存在与泌酸性萎缩相关，但以前没有明确的证据表明除了H。pylori感染能够诱导化生性改变（最近由Engstrand和Graham综述5）。然而，在Gut by Kwon等人的研究中，表明缺乏H.幽门螺杆菌可引起胃泌酸萎缩和化生，
The gastric mucosa is exposed to billions of diverse microorganisms every day. To stymie gastric colonisation as well as to limit passage of potential pathogens to more distal segments of the GI tract, the stomach has several broadly active defence mechanisms: acidity, mucus and proteolytic enzymes. Other extragastric mechanisms may contribute: for example, glycosylation epitopes like 3′-Sulfo-Lewis A on salivary mucins cotransit with swallowed bacteria and associate with them when the pH drops in the stomach, 1 presumably preventing the bacteria from binding the mucosa.Despite these defenses, at least one bacterial species, Helicobacter pylori is able to colonise the human stomach. This pathogen initially invades the gastric antrum, but it can also spread to the gastric body by inducing a metaplastic glandular response, 2 characterised by loss of acidsecreting parietal cells (oxyntic atrophy) and metaplastic glandular changes (ie, Spasmolytic Expressing Polypeptide Metaplasia or SPEM). In a small proportion of individuals, metaplasia can progress to dysplasia and gastric adenocarcinoma. Thus, identifying the early histological changes associated with H. pylori infection becomes clinically important. 3 The decrease in or absence of acidity associated with oxyntic atrophy creates an environment permissive for colonisation by opportunistic microbes. Although the presence of these ectopic microbial communities correlates with oxyntic atrophy, 4 previously there has been no clear demonstration that bacteria other than H. pylori were able to induce metaplastic changes (recently reviewed by Engstrand and Graham 5). However, in Gut by Kwon et al, show that microbial communities lacking H. pylori may give rise to oxyntic atrophy and metaplasia with subsequent
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DOI：
10.1038/nrgastro.2018.5
发表时间：
2018-05
期刊：
Nature reviews. Gastroenterology & hepatology
影响因子：
--
作者：
Sáenz JB;Mills JC
通讯作者：
Mills JC
影响因子：
12.2
作者：
Sheh, Alexander;Fox, James G.
通讯作者：
Fox, James G.
影响因子：
29.4
作者：
Burclaff J;Osaki LH;Liu D;Goldenring JR;Mills JC
通讯作者：
Mills JC
影响因子：
29.4
作者：
Petersen, Christine P.;Weis, Victoria G.;Goldenring, James R.
通讯作者：
Goldenring, James R.
影响因子：
29.4
作者：
Amieva M;Peek RM Jr
通讯作者：
Peek RM Jr