Intestinal Microbiome and Lymphoma Development

Yamamoto, Mitsuko L.; Schiestl, Robert H.

doi:10.1097/ppo.0000000000000047

Cited by 37 publications

(37 citation statements)

References 70 publications

(72 reference statements)

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“…Various risk factors including genetic and molecular alterations,3, 4, 5 diet,3, 6, 7 and chronic inflammation8, 9, 10 have been linked to the development of both disorders. Still other studies have suggested an association between chronic mucosal inflammation and the progression of IBD to pronounced dysplasia in the GI tract 11, 12, 13, 14…”

Section: Introductionmentioning

confidence: 98%

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Garraway

Johannes

Bryan

et al. 2018

Veterinary Internal Medicne

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BackgroundThe gastrointestinal (GI) microbiota in healthy cats is altered in IBD. Little research has been performed to identify whether specific bacterial groups are associated with small cell GI lymphoma (LSA).HypothesisMucosal bacteria, including Enterobacteriaceae and Fusobacterium spp., are abundant in intestinal biopsies of cats with small cell GI LSA compared to cats with IBD.AnimalsFourteen cats with IBD and 14 cats with small cell GI LSA.MethodsRetrospective case control study. A search of the medical records was performed to identify cats diagnosed with IBD and with GI LSA. Bacterial groups identified by FISH in GI biopsies were compared between cohorts and correlated to CD11b+ and NF‐κB expression.Results Fusobacterium spp. (median; IQR bacteria/region) were higher in cats with small cell GI LSA in ileal (527; 455.5 – 661.5; P = .046) and colonic (404.5; 328.8 – 455.5; P = .016) adherent mucus, and combined colonic compartments (free mucus, adherent mucus, attaching to epithelium) (8; 0 – 336; P = .017) compared to cats with IBD (ileum: 67; 31.5 – 259; colon: 142.5; 82.3 – 434.5; combined: 3; 0 – 34). Bacteroides spp. were higher in ileal adherent mucus (P = .036) and 3 combined ileal compartments (P = .034) of cats with small cell GI LSA. There were significant correlations between Fusobacterium spp. totals and CD11b+ cell (P = .009; rs .476) and NF‐κB expression (P = .004; rs .523).ConclusionsThe bacterial alterations appreciated might be influential in development of small cell GI LSA, and should drive further studies to elucidate the effects of microbial‐mediated inflammation on GI cancer progression.

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Section: Introductionmentioning

confidence: 98%

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Garraway

Johannes

Bryan

et al. 2018

Veterinary Internal Medicne

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“…44, 46, 47, 48, 49 Furthermore, S. bovis has also been associated with hematopoietic malignancy. 37, 50 It should be emphasized that despite the fact that oral cavity cancer, specifically squamous cell carcinoma, has been linked to numerous potential bacteria (examples include: Veillonella, Fusobacterium, Prevotella, Porphyromonas, Actinomyces, Clostridium, Haemophilus, Enterobacteriaceae, Streptococcus spp., and Gemella spp. ), no pathognomonic bacteria have yet been identified.…”

Section: Microbiome In Cancermentioning

confidence: 99%

“…Alterations in MAMPs trigger pattern receptors of innate immunity, including Toll-like receptors (TLR) and/or nucleotide-binding-oligomerization-domain (NOD)-like receptors. 37, 54 Stimulating the receptors activates the NF-κB pathway and causes expression of cytokines and interleukins.…”

Section: Microbiome In Cancermentioning

confidence: 99%

Microbiome and potential targets for chemoprevention of esophageal adenocarcinoma

Neto

Whitaker

Pei

2016

Seminars in Oncology

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Esophageal cancer is one of the deadliest cancers, with a dismal prognosis. It is increasingly recognized that esophageal cancer is a heterogeneous disease. It can be subdivided into two distinct groups: squamous cell carcinoma and adenocarcinoma, based on histological appearance. In the Western world, the incidence of squamous cell carcinoma was considerably higher than esophageal adenocarcinoma (EA) until the 1990s when, due to a dramatic increase, the incidence of EA surpassed that of squamous cell carcinoma. EA typically follows a well-established stepwise evolution from chronic inflammation due to reflux esophagitis (RE) that progresses to metaplasia (Barrett’s esophagus- BE) to dysplasia, which often culminates in EA. The pathophysiology of EA is complex and involves diverse factors, including gastroesophageal reflux, gastric acid secretion, dysfunction of the antireflux barrier, gastric emptying disturbances, and abnormalities in esophageal defense mechanisms. The current understanding of the etiology of EA is mainly derived from epidemiological studies of risk factors such as cigarette smoking, obesity, gastroesophageal reflux disorders (GERD), and low fruit and vegetable consumption. Numerous studies have been done but the factors that drive the dynamic increase in the incidence of EA remain elusive. The advent of widespread antibiotic use occurred in the 1950s, preceding the surge of EA. Based on this temporal sequence, it has been hypothesized that antibiotics alter the microbiome to which the esophagus is exposed in patients who have GERD and that chronic exposure to this abnormal microbiome (i.e., changes in species diversity or abundance) accounts for the increase in EA. If changes in the proposed factors alter the stepwise progression (RE-BE-dysplasia- EA), they may represent potential targets for chemoprevention. New discoveries will help improve our understanding of the biology and pathogenesis of these cancers, and aid in finding novel therapeutic targets.

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“…Since there is such a close interaction between these two players, it is not surprising that cancers of the immune system, e.g., lymphomas such as mucosal-associated lymphoid tissue (MALT) lymphomas have been shown to be caused by bacteria. These lymphomas originate in the marginal zone and 90% of MALT lymphomas are associated with the presence of Helicobacter ; elimination of Helicobacter leads to complete remission in approximately 80% of all cases(64). The causative effect of Helicobacter in MALT lymphomas has been demonstrated in animal models.…”

Section: Cancermentioning

confidence: 99%

Understanding Luminal Microorganisms and Their Potential Effectiveness in Treating Intestinal Inflammation

Ince

Blazar

Edmond

et al. 2016

Inflammatory Bowel Diseases

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The human intestine contains 1014 bacteria, which outnumber the mammalian cells 10-fold. Certain other commensal or infectious agents, like helminthic parasites become members of this microbial ecosystem, especially in populations living under less hygienic conditions. Intestinal microbes, also called the microbiome or microbiota, shape the host immune reactivity to self and nonself throughout life. Changes in microbiome composition may impair the maturation of immune regulatory pathways and predispose the host to develop various forms of inflammatory disorders, like Crohn's disease or ulcerative colitis. The microbiome is also critical to successful transplantation of organs or grafts. After allogeneic hematopoietic stem cell transplantation (HSCT), when the new donor cells, such as T lymphocytes learn to discriminate “the new-self from nonself” in the transplant recipient, they need healthy microbiota-derived signals to preserve the immune homeostasis. Restoring microbiota via intestinal delivery of bacterial strains, helminths, fecal microbiota transplantation or stool substitutes have the potential to improve and correct aberrant immune reactivity in various disorders.

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Intestinal Microbiome and Lymphoma Development

Cited by 37 publications

References 70 publications

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Relationship of the mucosal microbiota to gastrointestinal inflammation and small cell intestinal lymphoma in cats

Microbiome and potential targets for chemoprevention of esophageal adenocarcinoma

Understanding Luminal Microorganisms and Their Potential Effectiveness in Treating Intestinal Inflammation

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