Accumulation of Stimulants of Toll‐Like Receptor (TLR)‐2 and TLR4 in Meat Products Stored at 5 °C

Erridge, Clett

doi:10.1111/j.1750-3841.2010.02018.x

Cited by 25 publications

(32 citation statements)

References 41 publications

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“…The immune system includes LPS-detoxifying properties through the intestinal alkaline phosphatase (IAP)[17]. However, dietary LPS can trigger immune responses to the hosts due to their resistance to temperatures and low pH, even though their carriers (e.g., meat products, processed foods) are edible [15,18]. LPS-induced TLR4 activation leads to inflammation by secreting pro-inflammatory cytokines and chemokines.…”

Section: Introductionmentioning

confidence: 99%

Metabolic diseases and pro- and prebiotics: Mechanistic insights

Nakamura

Omaye

2012

Nutr Metab (Lond)

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Metabolic diseases, such as obesity and type 2 diabetes, are world-wide health problems. The prevalence of metabolic diseases is associated with dynamic changes in dietary macronutrient intake during the past decades. Based on national statistics and from a public health viewpoint, traditional approaches, such as diet and physical activity, have been unsuccessful in decreasing the prevalence of metabolic diseases. Since the approaches strongly rely on individual’s behavior and motivation, novel science-based strategies should be considered for prevention and therapy for the diseases. Metabolism and immune system are linked. Both overnutrition and infection result in inflammation through nutrient and pathogen sensing systems which recognize compounds with structural similarities. Dietary macronutrients (fats and sugars) can induce inflammation through activation of an innate immune receptor, Toll-like receptor 4 (TLR4). Long-term intake of diets high in fats and meats appear to induce chronic systemic low-grade inflammation, endotoxicity, and metabolic diseases. Recent investigations support the idea of the involvement of intestinal bacteria in host metabolism and preventative and therapeutic potentials of probiotic and prebiotic interventions for metabolic diseases. Specific intestinal bacteria seem to serve as lipopolysaccharide (LPS) sources through LPS and/or bacterial translocation into the circulation due to a vulnerable microbial barrier and increased intestinal permeability and to play a role in systemic inflammation and progression of metabolic diseases. This review focuses on mechanistic links between metabolic diseases (mainly obesity and type 2 diabetes), chronic systemic low-grade inflammation, intestinal environment, and nutrition and prospective views of probiotic and prebiotic interventions for the diseases.

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Section: Introductionmentioning

confidence: 99%

Metabolic diseases and pro- and prebiotics: Mechanistic insights

Nakamura

Omaye

2012

Nutr Metab (Lond)

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“…The research result of Westerners' diet showed that, in unprocessed food, the level of PAMPs is too low to detect. However, in processed food, it is much higher than the average level in small intestine [44].…”

Section: Gut Biological Barrier and Nafldmentioning

confidence: 97%

Role of gut barrier function in the pathogenesis of nonalcoholic fatty liver disease

Dai¹,

Lv²

2012

WCJD

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Nonalcoholic fatty liver disease (NAFLD) is one of the most common forms of chronic liver disease, and its incidence is increasing year by year. Many efforts have been made to investigate the pathogenesis of this disease. Since 1998 when Marshall proposed the conception of "gut-liver axis, " more and more researchers have paid close attention to the role of gut barrier function in the pathogenesis of NAFLD. The four aspects of gut barrier function, including physical, chemical, biological, and immunological barriers, are interrelated closely and related to NAFLD. In this paper, we present a summary of research findings on the relationship between gut barrier dysfunction and the development of NAFLD, aiming at illustrating the role of gut barrier function in the pathogenesis of this disease.

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“…Strategies for improved meat hygiene from "farm to fork" have been suggested by the FAO, the European Union, and the United States (53)(54)(55). Various methods to inactivate microorganisms in meat have been proposed (56-58); however, cooking of the meat may not destroy microbial-associated molecular patterns that may still be present even if the meat no longer contains living organisms (59).…”

Section: Discussionmentioning

confidence: 99%

Meat and fiber intake and interaction with pattern recognition receptors (TLR1, TLR2, TLR4, and TLR10) in relation to colorectal cancer in a Danish prospective, case-cohort study

Kopp

Vogel

Tjønneland

et al. 2018

The American Journal of Clinical Nutrition

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Background: Meat and dietary fiber are associated with increased and decreased risk of colorectal cancer (CRC), respectively. Toll-like receptors (TLRs) regulate the intestinal immune response in a complex interplay between the mucosal epithelium and the microbiota and may therefore be important modulators of diet-induced CRC together with other inflammatory mediators. Objective: Our aim was to investigate the association between functional TLR polymorphisms and risk of CRC and the interaction with dietary factors. Additionally, interactions with previously studied polymorphisms in IL10, IL1B, PTGS2, and NFKB1 were assessed in order to examine possible biological pathways in meat-induced CRC. Design: A nested case-cohort study of 897 CRC cases and 1689 randomly selected participants from the Danish prospective "Diet, Cancer and Health" study encompassing 57,053 persons was performed using Cox proportional hazard models and the likelihood ratio test. Results: We found associations between polymorphisms in TLR2 (P = 0.018) and TLR4 (P = 0.044) and risk of CRC per se, interactions between intake of red and processed meat (10 g/d) and polymorphisms in TLR1 (P-interaction = 0.032) and TLR10 (P-interaction = 0.026 and 0.036), and intake of cereals (50 g/d) and TLR4 (P-interaction = 0.044) in relation to risk of CRC. Intake of red and processed meat also interacted with combinations of polymorphisms in TLR1 and TLR10 and polymorphisms in NFKB1, IL10, IL1B, and PTGS2 (P-interaction; TLR1/rs4833095 × PTGS2/rs20417 = 0.021, TLR10/rs11096955 × IL10/rs3024505 = 0.047, TLR10/rs11096955 × PTGS2/rs20417 = 0.017, TLR10/rs4129009 × NFKB1/rs28362491 = 0.027, TLR10/rs4129009 × IL1B/rs4848306 = 0.020, TLR10/rs4129009 × IL1B/rs1143623 = 0.021, TLR10/rs4129009 × PTGS2/rs20417 = 0.027), whereas intake of dietary fiber (10 g/d) interacted with combinations of polymorphisms in TLR4, IL10, and PTGS2 (P-interaction; TLR4/rs1554973 × IL10/rs3024505 = 0.0012, TLR4/rs1554973 × PTGS2/rs20417 = 0.0041, TLR4/rs1554973 × PTGS2/rs5275 = 0.0064). Conclusions: Our study suggests that meat intake may activate TLRs at the epithelial surface, leading to CRC via inflammation by nuclear transcription factor-κB-initiated transcription of inflammatory genes, whereas intake of fiber may protect against CRC via TLR4-mediated secretion of interleukin-10 and cyclooxygenase-2. Our results should be replicated in other prospective cohorts with well-characterized participants. The trial was registered at www.clinicaltrials.gov as NCT03250637.Am J Clin Nutr 2018;107:465-479.

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Accumulation of Stimulants of Toll‐Like Receptor (TLR)‐2 and TLR4 in Meat Products Stored at 5 °C

Cited by 25 publications

References 41 publications

Metabolic diseases and pro- and prebiotics: Mechanistic insights

Metabolic diseases and pro- and prebiotics: Mechanistic insights

Role of gut barrier function in the pathogenesis of nonalcoholic fatty liver disease

Meat and fiber intake and interaction with pattern recognition receptors (TLR1, TLR2, TLR4, and TLR10) in relation to colorectal cancer in a Danish prospective, case-cohort study

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