• Keywords
• NOD mouse, beta-cell stress, enterovirus, environmental factors, gluten-free diet, gut-pancreas axis, intestinal permeability, type 1 diabetes,
• MeSH
• Abdomen MeSH
• Diabetes Mellitus, Type 1 * MeSH
• Humans MeSH
• Pancreas MeSH
• Check Tag
• Humans MeSH
• Publication type
• Editorial MeSH

Inflammatory processes play an important role in the development of nasal polyps (NP), but the etiology and, to a high degree also, the pathogenesis of NP are not fully understood. The role of several cytokines and chemokines such as eotaxins, IL-4, IL-5, IL-6, IL-8, and RANTES has been reported in NP. Herewith, we investigated the expression and pattern of distribution of chemokine receptors CCR1 and CCR3 in nasal polyps. Immunohistochemical detection was carried out in frozen sections of biopsies from 22 NP and 18 nasal mucosa specimens in both the epithelial and stromal compartments. Fluorescence microscopy and computerized image analysis revealed a statistically significant increased number of CCR1 (45.2 ± 2.8 vs. 15.1 ± 1.9, p < 0.001)-positive as well as CCR3 (16.4 ± 1.4 vs. 9.7 ± 1.1, p < 0.001)-positive cells in the stroma of NP compared to nasal mucosa. In comparison to healthy nasal mucosa, increased positivity of CCR3 was detected in the epithelial compartment of NP. Our data suggest that increased expression of CCR1 and CCR3 chemokine receptors may, in accord with various chemokines, contribute to the pathogenesis of nasal polyposis by facilitating increased migration and prolonged accumulation of inflammatory cells, e.g., eosinophils, in the inflammatory infiltrate of NP.

• MeSH
• Eosinophils cytology   MeSH
• Granulocytes cytology   MeSH
• Humans MeSH
• Nasal Polyps genetics   metabolism   pathology   MeSH
• Nasal Mucosa metabolism   pathology   MeSH
• Receptors, CCR1 genetics   metabolism   MeSH
• Receptors, CCR3 genetics   metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• CCR1 protein, human MeSH Browser
• CCR3 protein, human MeSH Browser
• Receptors, CCR1 MeSH
• Receptors, CCR3 MeSH

Metagenomic approaches are currently being used to decipher the genome of the microbiota (microbiome), and, in parallel, functional studies are being performed to analyze the effects of the microbiota on the host. Gnotobiological methods are an indispensable tool for studying the consequences of bacterial colonization. Animals used as models of human diseases can be maintained in sterile conditions (isolators used for germ-free rearing) and specifically colonized with defined microbes (including non-cultivable commensal bacteria). The effects of the germ-free state or the effects of colonization on disease initiation and maintenance can be observed in these models. Using this approach we demonstrated direct involvement of components of the microbiota in chronic intestinal inflammation and development of colonic neoplasia (i.e., using models of human inflammatory bowel disease and colorectal carcinoma). In contrast, a protective effect of microbiota colonization was demonstrated for the development of autoimmune diabetes in non-obese diabetic (NOD) mice. Interestingly, the development of atherosclerosis in germ-free apolipoprotein E (ApoE)-deficient mice fed by a standard low-cholesterol diet is accelerated compared with conventionally reared animals. Mucosal induction of tolerance to allergen Bet v1 was not influenced by the presence or absence of microbiota. Identification of components of the microbiota and elucidation of the molecular mechanisms of their action in inducing pathological changes or exerting beneficial, disease-protective activities could aid in our ability to influence the composition of the microbiota and to find bacterial strains and components (e.g., probiotics and prebiotics) whose administration may aid in disease prevention and treatment.

• MeSH
• Autoimmune Diseases etiology   microbiology   MeSH
• Gastrointestinal Tract microbiology   MeSH
• Germ-Free Life * MeSH
• Immunity MeSH
• Humans MeSH
• Metagenome immunology   MeSH
• Disease Models, Animal MeSH
• Neoplasms etiology   microbiology   MeSH
• Mucous Membrane immunology   MeSH
• Inflammation etiology   microbiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH

Our study examined whether repeated preventive oral administration of live probiotic bacterial strains Escherichia coli O83:K24:H31 (Ec O83), Escherichia coli Nissle 1917 O6:K5:H1 (Ec Nis) and Lactobacillus casei DN 114001 (Lc) can protect mice against dextran sodium sulfate (DSS)-induced colitis. A significant decrease in average symptom score was observed in Ec O83-, Ec Nis- and Lc-pretreated group (p < 0.05). Significant differences in body mass loss between Lc pretreated mice with DSS-induced colitis were found when compared with nontreated mice (p < 0.05). PBS pretreated mice had a significantly shorter colon than Ec O83-, Ec Nis- and Lc-pretreated mice (p < 0.05). Administration of Lc significantly decreased the severity of DSS induced histological marks of inflammation (p < 0.05). A significant difference (p < 0.05) was also found in specific IgA level against given probiotic in enteral fluid between colitic mice and healthy mice pretreated with Ec 083 and Ec Nis.

• MeSH
• Administration, Oral MeSH
• Escherichia coli MeSH
• Histocytochemistry MeSH
• Immunoglobulin A analysis   MeSH
• Colon microbiology   MeSH
• Lacticaseibacillus casei MeSH
• Disease Models, Animal MeSH
• Mice, Inbred BALB C MeSH
• Mice MeSH
• Probiotics pharmacology   MeSH
• Dextran Sulfate adverse effects   MeSH
• Intestinal Mucosa immunology   pathology   MeSH
• Colitis, Ulcerative chemically induced   immunology   prevention & control   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Immunoglobulin A MeSH
• Dextran Sulfate MeSH

Some patients with immunodeficiency develop clinical features of autoimmune disorders. A previously asymptomatic antibody deficiency can underlie the development of autoimmune diseases and a severe course of infection, with a risk of sepsis; such cases are known in selective IgA deficiency. On the other hand, little information is available on selective IgG subclass deficiencies. An unexpectedly severe course of Campylobacter infection in a 19-year-old woman with a previously undiagnosed complex immune disorder, including selective IgG1 immunodeficiency, Hashimoto's autoimmune thyroiditis with hypothyroidism combined with Addison's disease presumably due to autoimmune adrenalitis, autoimmunity and allergy is described. The pathophysiological mechanisms of autoimmunity in latent humoral defects are discussed.

• MeSH
• Addison Disease complications   MeSH
• Hypersensitivity complications   MeSH
• Campylobacter jejuni isolation & purification   MeSH
• IgG Deficiency complications   MeSH
• Adult MeSH
• Hashimoto Disease complications   MeSH
• Campylobacter Infections complications   microbiology   MeSH
• Humans MeSH
• Multiple Organ Failure * MeSH
• Sepsis complications   microbiology   MeSH
• Check Tag
• Adult MeSH
• Humans MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Case Reports MeSH
• Research Support, Non-U.S. Gov't MeSH

The prevalence of celiac disease (CD) was determined in healthy blood donors and in high-risk groups of adults (a total of 1835 adults--randomly selected 1312 healthy blood donors, 102 patients with primary osteoporosis, 58 patients with autoimmune diseases and 365 infertile women). It was calculated on the basis of a two-step serologic screening method--in the first step IgA and IgG antigliadin antibodies (AGA) and IgA anti-gamma-glutamyltransferase ('transglutaminase') antibodies (ATG) were estimated, in the second step sera positive for IgA AGA and/or IgA ATG were examined for antiendomysial IgA (AEA) antibodies. Immunoenzymic assay (ELISA) was used for determining of AGA and ATG antibodies; immunofluorescence method, performed on human umbilical cord tissue, was used for assaying of AEA antibodies. Total serum IgA level in only IgG AGA positive subjects was measured by routine turbidimetric method. 0.45% of healthy blood donors, 0.98% of osteoporotic patients, 2.7% of patients suffering from autoimmune disease and 1.13% of women with infertility considered as immunologically mediated were found to be positive in both steps of serologic screening (AGA and/or ATG and antiendomysium positive). The presumed high prevalence of seropositivity for CD in apparently healthy Czech adult population was confirmed. In the high-risk groups, the prevalence of seropositivity for CD was approximately 2-4 times higher than in healthy blood donors. The real prevalence of CD in the tested groups, however, can be estimated after performing small intestinal biopsy in the seropositive patients.

• MeSH
• Autoimmune Diseases complications   MeSH
• Celiac Disease complications   diagnosis   epidemiology   immunology   MeSH
• Adult MeSH
• Enzyme-Linked Immunosorbent Assay MeSH
• gamma-Glutamyltransferase immunology   MeSH
• Gliadin immunology   MeSH
• Immunoglobulin A blood   MeSH
• Immunoglobulin G blood   MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Osteoporosis complications   MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Seroepidemiologic Studies MeSH
• Infertility, Female complications   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Adolescent MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Geographicals
• Czech Republic epidemiology   MeSH
• Names of Substances
• gamma-Glutamyltransferase MeSH
• Gliadin MeSH
• Immunoglobulin A MeSH
• Immunoglobulin G MeSH

One-week dextran sulfate treatment of conventional (CV) immunodeficient (SCID) mice gave rise to acute colitis in the colon mucosa; germ-free (GF) SCID mice did not exhibit any changes in colon morphology. Dextran sulfate application to CV immunocompetent (BALB/c) mice did induce substantial changes in the colon mucosa (grade 4); GF BALB/c mice showed mild changes in the colon morphology (grade 1) only. GF SCID mice and CV SCID mice died during the second round of dextran sulfate treatment suffering from chronic colitis; GF BALB/c mice exhibited mild crypt distortion while CV BALB/c mice showed a complete loss of the surface epithelium (grade 4), accompanied by T and B lymphocyte infiltration.

• MeSH
• Immunocompetence * MeSH
• Colitis chemically induced   microbiology   pathology   MeSH
• Colon microbiology   pathology   MeSH
• Disease Models, Animal MeSH
• Mice, Inbred BALB C MeSH
• Mice, SCID MeSH
• Mice MeSH
• Specific Pathogen-Free Organisms MeSH
• Dextran Sulfate MeSH
• Intestinal Mucosa pathology   MeSH
• Inflammation pathology   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Research Support, U.S. Gov't, P.H.S. MeSH
• Comparative Study MeSH
• Names of Substances
• Dextran Sulfate MeSH