The small intestine
Paul Ong, Rachel Skittrall in Gastrointestinal Nursing, 2017
One of the most important environmental triggers that seems to affect the pathophysiology of Crohn's disease is food. Sakamoto et al. (2005) and Tsujikawa et al. (2001) found that diets that contained a lot of fat and sugar accelerated the onset of Crohn's disease. A number of studies have also suggested that intestinal flora play a key role in triggering the onset of inflammation. It is believed that the adherence and invasion of pathogenic Escherichia coli (E. coli) into the intestinal mucosa brings on the development of the disease (Fellermann et al., 2003). Under normal circumstances the body's innate defence mechanisms would prevent bacteria crossing into the intestinal mucosa. However Fellermann et al. (2003) believes that the mutated and defective CARD15/NOD2 gene identified earlier could lead to a breakdown in the body's innate defence responses leading to the invasion of bacteria into intestinal mucosa, bringing about an inflammatory response.
Anisakis, Allergy and the Globalization of Food
Andreas L. Lopata in Food Allergy, 2017
Food-borne illnesses are estimated to kill more than 2 million people annually and impedes economies by removing healthy workers from the workforce and in developing countries, causing a cycle of malnutrition and illness (World Health Organization 2014a, World Health Organization 2014b). The most common foodborne pathogens are Salmonella, Campylobacter and enterohaemorrhagic Escherichia coli which are well known by the general public due to local health education initiatives (World Health Organization 2014a,b). Other food-borne pathogens such as viruses and parasites are often not considered in the local context due to high local food standards and regulations; however the global supply chain allows yearlong availability of seasonal produce sourced from around the world. Therefore, other pathogens such as the nematode Anisakis, need to be considered when a patient presents with gastrointestinal symptoms and particularly if they subsequently develop a food allergy. This chapter will explore how Anisakis species and its associated illness, anisakiasis, should be considered by clinicians outside of endemic areas and how food globalization have contributed to this situation.
Epidemiology, Disease Transmission, Prevention, and Control
Julius P. Kreier in Infection, Resistance, and Immunity, 2022
Food-borne disease causes significant illness in people in both developed and underdeveloped countries. The microorganisms responsible include viruses, bacteria, protozoa, and worms. Morbidity depends on the pathogen, the susceptibility of the infected humans, and the medical care available. Diarrheal diseases have a strong cyclical occurrence. Higher temperatures favor the prevalence of food-borne illnesses caused by pathogens that replicate on foods at high ambient temperatures. Production of staphylococcal toxins, a common contaminant of food is also associated with high temperature. Other bacteria that are food contaminants are Campylobacter jejuni, which is acquired by drinking contaminated milk or water or by eating improperly cooked poultry meat, and Escherichia coli 0157:H7 by eating undercooked meat. Salmonella, Shigella, and Vibrio cholerae, as well as Cryptosporidium parvum, Cyclospora cayetanenis, and Trichenella spiralis are also transmitted by food.
Bacterial imbalance and gut pathologies: Association and contribution of E. coli in inflammatory bowel disease
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Shahanavaj Khan, Ahamad Imran, Abdul Malik, Anis Ahmad Chaudhary, Abdur Rub, Arif Tasleem Jan, Jakeera Begum Syed, Christian Rolfo
Escherichia coli (E. coli) is a gram-negative bacterium that normally resides in the intestine of humans and many animals [10]. Although most strains of E. coli are not injurious, several strains produce toxins during infection that can cause diarrhea, fever, urinary tract infections pain, and intestinal cancer [11,12]. In 1998, a study detected a new pathogenic E. coli strain in inflamed intestine tissues of CD patients [13]. However, diagnosis of such E. coli was performed mostly via phenotypic-based classical immunological assays, not molecular assays such as polymerase chain reaction or restriction digestion of specific virulence genes [14]. Uropathogenic E. coli serotypes were identified in many patients with UC flares in the 1970s [15]. E. coli are generally classified into A, B1, B2, and D phylogenetic groups. Commensal strains are found in the A and B1 groups, which carry only a few virulence genes, while the B2 and D pathogenic groups generally have many virulence genes that support adhesion and persistent extra-intestinal infection [16]. Furthermore, the B2 E. coli group was shown to exhibit extra-intestinal pathogenic potential (ExPEC) due to the large number of virulence genes, and was found to be abundant in active UC patients [17]. Therefore, alterations in the diversity, richness, and stability of the bacterial ecosystem in host intestines are associated with gut pathologies including IBD and CRC.
Myosin light chain kinase regulates intestinal permeability of mucosal homeostasis in Crohn’s disease
Published in Expert Review of Clinical Immunology, 2020
Yiran Yao, Qi Feng, Jun Shen
Some researchers consider IBD as a disease of impaired barrier [129]. The term ‘mucosal barrier’ appropriately emphasizes the critical shielding and resistance function of the intestinal mucosa in its interaction with the microbiota [13]. For example, the imbalance of intestinal Escherichia coli microbiota influences intestinal permeability and CD pathogenesis [130]. Escherichia coli is a group of intestinal colonization bacteria, most of which are harmless to the human body. Among them, adhesion invasive Escherichia coli (AIEC) could selectively target TJ protein, resulting in insult to the intestinal barrier. When the intestinal barrier is impaired, AIEC is internalized and replicated, leading to further deterioration of the intestinal barrier function. Inflammation acts as a leading role in the damage to the intestinal barrier. In particular, AIEC directly or indirectly activates TNF-α/NF-κB/MLCK pathway to increase intestinal permeability. However, when probiotics overcome pathogens, they may restore microbial balance, TJ complex, and intestinal permeability. Which provide a potential therapy to restore barrier function in CD [131].
Phosphodiesterase 5 (PDE5) restricts intracellular cGMP accumulation during enterotoxigenic Escherichia coli infection
Published in Gut Microbes, 2020
Jennifer Foulke-Abel, Huimin Yu, Laxmi Sunuwar, Ruxian Lin, James M. Fleckenstein, James B. Kaper, Mark Donowitz
The Global Enteric Multi-Center Study (GEMS) identified enterotoxigenic Escherichia coli (ETEC) infection as one of the four leading causes of acute diarrhea and associated mortalities in developing countries.1 As the leading cause of traveler’s diarrhea, ETEC is also a recognized burden on deployed U.S. military personnel.2 The host diarrheal response is initiated by the secreted peptide heat-stable enterotoxin (ST) and/or the multi-subunit protein heat-labile enterotoxin (LT) via induction of second messenger cGMP and cAMP synthesis, respectively. ETEC strain H10407, originally isolated from a patient in Bangladesh with severe cholera-like diarrhea,3 employs additional factors to facilitate host interaction, including but not limited to the secreted mucinase EatA4 and surface adhesins EtpA5,6 and CfaE.7 Strains expressing ST, alone or in combination with LT, were more highly associated with diarrhea than LT-only expressing strains,8 confirming the importance of ST in disease pathogenesis. As such, recent renewed efforts to employ ST antigens for vaccine development are under way.9,10
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