Abstract
Chronic inflammation and long-term tissue injury are related to many malignancies, including gastric cancer (GC). Helicobacter pylori (H. pylori), classified as a class I carcinogen, induces chronic superficial gastritis followed by gastric carcinogenesis. Despite a high prevalence of H. pylori infection, only about 1–3% of people infected with this bacterium develop GC worldwide. Furthermore, the development of chronic gastritis in some, but not all, H. pylori-infected subjects remains unexplained. These conflicting findings indicate that clinical outcomes of aggressive inflammation (atrophic gastritis) to gastric carcinogenesis are influenced by several other factors (in addition to H. pylori infection), such as gut microbiota, co-existence of intestinal helminths, dietary habits, and host genetic factors. This review has five goals: (1) to assess our current understanding of the process of H. pylori-triggered inflammation and gastric precursor lesions; (2) to present a hypothesis on risk modulation by the gut microbiota and infestation with intestinal helminths; (3) to identify the dietary behavior of the people at risk of GC; (4) to check the inflammation-related genetic polymorphisms and role of exosomes together with other factors as initiators of precancerous lesions and gastric carcinoma; and (5) finally, to conclude and suggest a new direction for future research.
Highlights
Gastric cancer (GC) is the most common cancer contributing to 5.5% of all new cases of cancers
It proceeds from normal mucosa infected with H. pylori to chronic active gastritis, atrophic gastritis (AG), intestinal metaplasia, dysplasia, hyperplasia, and adenocarcinoma [7,8,9,10]
These findings suggest that early childhood exposure to intestinal helminths induces immunoregulatory lymphocytes and anti-inflammatory cytokines such as IL-4, IL-10, and TGF-β and lowers the expression of pro-inflammatory IFN-γ, TNF-α, and IL-1β, including Th1-associated IP-10, RANTES, and MIP-1β
Summary
Gastric cancer (GC) is the most common cancer contributing to 5.5% of all new cases of cancers. A study on gastric mucosal samples showed decreased expression of proinflammatory cytokines and predominant Th2 response (higher level IL-4) among H. pylori-infected humans coinfected with intestinal helminthes [81]. A study on children from regions of low versus high risk of GC but similar H. pylori seropositivity showed that subjects from the low-risk area were more commonly infected with helminths and showed higher Th2-associated IgG1 responses to H. pylori infection [84] These findings suggest that early childhood exposure to intestinal helminths induces immunoregulatory lymphocytes and anti-inflammatory cytokines such as IL-4, IL-10, and TGF-β and lowers the expression of pro-inflammatory IFN-γ, TNF-α, and IL-1β, including Th1-associated IP-10, RANTES, and MIP-1β. HHyyppootthheessiissoonnththeeimimppacatcot focfoc-oe-xeixstiestnecnecoefoHf.Hpy. lpoyriloarni danindteinsttiensatlinhaellmheinlmthisn:tbhos:thboHt.hpyHlo. rpiyalnordi ianntdesitnintaelsthienlaml ihnetlhminfinecthtioinnfienctteioranctininteeraarcltyincheialdrlhyocohdi,ldrehsouoldtin, rgeisnulcthinagngine icnhaTnhg1ereinspTohn1serecsapuosnedsebcyauHs.epdylboyriHpr.ipmylaorriilypruipmreagriulylautiporneogfutluamtioonr onfectruomsiosrfancetcorros(TisNfaFc)-toαr, (iTnNteFrl)e-uαk,inin(tIeLrl)e-1ukαi/nβ(I,LIL)--16,αI/Lβ-,8I,LI-L6-,1I7L,-I8L, -I2L3-1a7n,dILm-2o3noancydtemcohneomcyotaettcrhacetmanotatptrroactetainnt(MprCoPte-i1n) (laaMstiwConPel-lo1af) saILsa-cw4ti,evIlaLl ta-i1so0na,coTtifrvananetsiuoftonrromopfihnnigleuagntrrdoopwmhtaihlcarfoancpdthomarga(eTcrGaonFpd)h-βaTghae2n-adpnoddloaTwrhizn2i-rnpeggoulraelrasiptzioionnngsoerfebsiypntohenerslfmeerbionynthh(eIeFslmNmi)n-aγit,nhTleysNumFp-aαrien,glayunludaptiIroLen-g1uoβf-, iInLc-4lu, dILin-1g0T, hTr1a-ansssfoocrimatiendgignrtoerwfethrofnacgtaomr (mTaG-Fin)d-βucaenddpdroowteninre1g0u(lIaPt-i1o0n),oRf eingtuelrafteerdonon(IAFNct)iv-γa,tiToNn,FN-αo,ramnadl TILE-1xβp,reinscseluddainndg TSehc1r-eatsesdoc(RiaAteNdTinEtSe)rfperrootneigna, manmdaM-inadcruocpehdapgreoitnefilnam10m(IaPto-1r0y),pRroetgeuinla(tMedIPo)n-1Aβ.ctTivhautsi,oTn,rNegourlmataolrTy (ETxrperge)srseesdpaonndseSienchreibteitds (tRheAdNeTvEelSo)ppmroentetionf, aatnrdopMhiaccgroaspthriatgiseainndflapmosmsiabtloyrlyowpreorsteciann(cMerIPri)s-k1βin. lTatheursl,ifTe (raefgteurla4t0o–r5y0 (yTeraergs)).response inhibits the development of atrophic gastritis and possibly lowers cancer risk in later life (after 40–50 years)
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