suggested that molecular mimicry may play a pathogenic role, i.e., immunological cross-reactivity between antigenic epitopes of viral proteins and gliadins via shared antigenic determinants. disease are discussed. spp. and Enterobacteriaceae while potentially protective bacteria (spp. and the group) are decreased in CD patients [32,34,35,36]. 2. Bacterial Infections in Celiac Disease Infectious diseases are associated with both increased morbidity and mortality in CD patients [37]. The increased susceptibility of CD patients to infections Rabbit polyclonal to Synaptotagmin.SYT2 May have a regulatory role in the membrane interactions during trafficking of synaptic vesicles at the active zone of the synapse. is probably explainable, even beyond the Midodrine hydrochloride genetically decided aberration of immune system functions, by impaired nutritional conditions, malnutrition, deficiency of vitamin D, folic acid, B12, hyposplenism, and altered mucosal intestinal permeability [38,39,40,41,42,43]. It is assumed that recurrent infections increase the risk of CD development [44,45]. Children suffering from more than ten gastrointestinal (or respiratory) infections are at a higher risk of CD development compared to children with less than four contamination events during the reference period [21,45]. Additionally, mucosal infections may contribute to the impairment of immune tolerance to gluten, leading to tissue damage in CD patients [46]. Infections, mainly those induced by and (was found in CD patients compared to controls. A higher incidence of contamination in CD was found in a large-scale population-based cohort study involving more than 28 thousand CD patients and more than 141 thousand controls; the incidence of contamination in the former group was estimated at 56/100,000 person-years in contrast to the incidence of 26/100,000 in controls (i.e., the general populace and non-CD controls). Interestingly, the risk of contamination was highest in the first 12 months after diagnosis (hazard ratio: 5.2, 0.0001) and remained high, for up to five years, compared to controls [47]. There is a risk of CD in children suffering from peptic ulcers: contamination was present in 63% of patients with Midodrine hydrochloride CD and 44% of non-celiac peptic ulcers; however, the difference was not statistically significant. Of the entire ulcer group, 11% of CD patients with peptic ulcers were negative for contamination [48]. The and genera were highly abundant in duodenal biopsy samples from adult CD patients compared to first-degree relatives and controls [49]. However, the role of these bacteria in the pathogenesis of CD has not been completely elucidated. It is a matter of debate whether these bacteria elicit pathological changes in the small gut mucosa of the celiac patients or the presence of these bacteria, due to immune dysregulation or intrinsic conditions in celiac patients, favor colonization by these bacterial species [30]. Nonetheless, CD patients are at increased risk for Midodrine hydrochloride the development of bacterial infections [50]. There are also rare reports on CD patients with respiratory diseases; a Swedish population-based 2006 study reported that this tuberculosis risk was 3C4 occasions higher in CD patients [51,52]. CD is associated with an increased risk of pneumococcal contamination. Invasive (is usually a causative agent of pneumonia, bacterial meningitis, and sepsis. One of the first comprehensive studies concerning pneumococcal contamination was performed in England. The objective of the study was to determine the risk (rate ratio) of pneumococcal contamination in patients with CD in a populace in: (1) the Oxford region (1963C1999); and (2) the whole of England (1998C2003). The high rate of pneumococcal infections in CD patients persisted beyond the first year after the CD diagnosis. It should be noted that this pneumococcal vaccination was available at the time of the all-England study but not at the time of the Oxford study, which influenced study conditions [42]. A Swedish study by R?ckert Tjernberg et al. [41] showed an increased risk (although statistically insignificant) of invasive pneumococcal disease in CD. The risk estimate was comparable after considering comorbidities, socioeconomic status, and education level [41]. An increased risk of bacterial pneumonia, especially in children and young people with CD, was found by Simons et al. [40] and Canova et al. [53]. Interestingly, the risk of bacterial pneumonia was significantly increased before the CD diagnosis [40,53]. For this reason, pneumococcal vaccination in individuals at risk of developing CD is the most effective way to prevent streptococcal pneumonia. Preventive pneumococcal vaccination should be considered for CD patients between 15 and 64 years who have not received the pneumococcal vaccination series in childhood [40]. The beneficial effect of the vaccination in CD, however, depends on splenic function [54]. Studies have reported a high prevalence of respiratory tract infections in CD patients with hyposplenism. Hyposplenism, along with malnutrition and vitamin deficiency, is the leading cause of susceptibility to respiratory infections such as streptococcal pneumonia. Interestingly, hyposplenism in adult CD patients ranges 19C80%.
