scholarly journals Muc5ac Expression Protects the Colonic Barrier in Experimental Colitis

2020 ◽  
Vol 26 (9) ◽  
pp. 1353-1367
Author(s):  
Kristine E Olli ◽  
Caroline Rapp ◽  
Lauren O’Connell ◽  
Colm B Collins ◽  
Eoin N McNamee ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
Antibiotic Treatment ◽  
Functional Role ◽  
Intestinal Helminth ◽  
Rrna Gene ◽  
Mesenteric Lymph Nodes ◽  
Murine Colitis ◽  
Dss Colitis ◽  
Mesenteric Lymph

Abstract Background The mucus gel layer (MGL) lining the colon is integral to exclusion of bacteria and maintaining intestinal homeostasis in health and disease. Some MGL defects allowing bacteria to directly contact the colonic surface are commonly observed in ulcerative colitis (UC). The major macromolecular component of the colonic MGL is the secreted gel-forming mucin MUC2, whose expression is essential for homeostasis in health. In UC, another gel-forming mucin, MUC5AC, is induced. In mice, Muc5ac is protective during intestinal helminth infection. Here we tested the expression and functional role of MUC5AC/Muc5ac in UC biopsies and murine colitis. Methods We measured MUC5AC/Muc5ac expression in UC biopsies and in dextran sulfate sodium (DSS) colitis. We performed DSS colitis in mice deficient in Muc5ac (Muc5ac-/-) to model the potential functional role of Muc5ac in colitis. To assess MGL integrity, we quantified bacterial-epithelial interaction and translocation to mesenteric lymph nodes. Antibiotic treatment and 16S rRNA gene sequencing were performed to directly investigate the role of bacteria in murine colitis. Results Colonic MUC5AC/Muc5ac mRNA expression increased significantly in active UC and murine colitis. Muc5ac-/- mice experienced worsened injury and inflammation in DSS colitis compared with control mice. This result was associated with increased bacterial-epithelial contact and translocation to the mesenteric lymph nodes. However, no change in microbial abundance or community composition was noted. Antibiotic treatment normalized colitis severity in Muc5ac-/- mice to that of antibiotic-treated control mice. Conclusions MUC5AC/Muc5ac induction in the acutely inflamed colon controls injury by reducing bacterial breach of the MGL.

scholarly journals P075 Muc5ac expression protects the colonic barrier in experimental colitis

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S173-S173
Author(s):  
L O’Connell ◽  
K Olli ◽  
C Rapp ◽  
C Collins ◽  
E McNamee ◽  
...  
Keyword(s):  
Antibiotic Treatment ◽  
Functional Role ◽  
Intestinal Barrier ◽  
Experimental Colitis ◽  
Intestinal Helminth ◽  
Mesenteric Lymph Nodes ◽  
Murine Colitis ◽  
Dss Colitis ◽  
Mucus Gel

Abstract Background The mucus gel layer (MGL) lining the colon is integral to exclusion of bacteria and maintaining intestinal homeostasis in health and disease. MGL defects allowing bacteria to directly contact the colonic surface are commonly observed in ulcerative colitis (UC). The major macromolecular component of the colonic MGL is the secreted gel-forming mucin, MUC2, whose expression is essential for homeostasis in health. In UC, another gel-forming mucin, MUC5AC is induced. In mice, Muc5ac is protective during intestinal helminth infection. Here, we tested the expression and functional role of MUC5AC/Muc5ac in colitis patient biopsies and murine colitis. Methods We measured MUC5AC/Muc5ac expression in UC patient biopsies and during acute dextran sulphate sodium (DSS) colitis. We performed DSS-colitis in mice deficient in Muc5ac (Muc5ac−/−) to model the potential functional role of Muc5ac in colitis. To assess MGL integrity, we quantified bacterial–epithelial interaction and translocation to mesenteric lymph nodes (MLNs). Antibiotic treatment was performed to directly investigate the role of colonic bacteria in our murine colitis studies. Results Colonic MUC5AC/Muc5ac mRNA expression increased significantly in active UC and murine colitis. Muc5ac−/− mice experienced worsened injury and inflammation in DSS-colitis compared with controls. This was associated with increased bacterial–epithelial contact and translocation to the MLN. Antibiotic treatment normalised colitis severity in Muc5ac−/− mice to that of antibiotic treated controls. Conclusion We demonstrate for the first time that MUC5AC/Muc5ac induction in acute colitis controls injury by reducing bacterial breach of the MGL. Therefore, developing strategies to induce MUC5AC expression may protect the intestinal barrier in UC.

Salmonella spp. in Healthy Swine and in Abattoir Environments in Brazil

1997 ◽  
Vol 60 (9) ◽  
pp. 1029-1033 ◽  
Author(s):  
NORMA S. LÁZARO ◽  
ANITA TIBANA ◽  
ERNESTO HOFER
Keyword(s):  
Lymph Nodes ◽  
Environmental Samples ◽  
The Other ◽  
Mesenteric Lymph Nodes ◽  
Salmonella Spp ◽  
Mesenteric Lymph ◽  
Hygienic Measures ◽  
And Storage ◽  
Tank Water

Tonsils and inguinal, mesenteric, and prescapular lymph node samples collected from 115 swine carcasses from two abattoirs and a family-run operation in the State of Rio de Janeiro, Brazil, were cultured for the presence of Salmonella species. Salmonella spp. were detected in 40 (34.8%) of the swine samples with the following distribution; tonsils (31/40, 77.5%), mesenteric lymph nodes (16/40, 40.0%), inguinal lymph nodes, (9/40, 22.5%), and prescapular lymph nodes (7/40, 17.5%), Scalding tank water and environmental swabs collected from the abattoirs were also analyzed. Salmonella spp. were recovered from 13 of 51 (22.5%) of the environmental samples from one of the two abattoirs, none from those from the other abattoir. Salmonella spp. were recovered from the evisceration tables (5/11, 45.5%), the killing room (3/10, 30.0%), the holding pen (2/10, 20.0%), the butchering saw (2/10, 20.0%), and the scalding tank (1/10, 10.0%). The most frequently detected serovar was Salmonella Muenster. The results show the necessity of adopting more effective hygienic measures in the abattoirs as well as in the areas where swine are raised in order to reduce the role of abattoirs and storage facilities in the spread of Salmonella contamination.

scholarly journals Longitudinal Study of Salmonella Dispersion and the Role of Environmental Contamination in Commercial Swine Production Systems

2009 ◽  
Vol 75 (6) ◽  
pp. 1478-1486 ◽  
Author(s):  
Paul M. Dorr ◽  
Daniel A. Tadesse ◽  
Bayleyegn Molla Zewde ◽  
Pamela Fry ◽  
Siddhartha Thakur ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
Susceptibility Testing ◽  
Fragment Length Polymorphism ◽  
Production Systems ◽  
Swine Production ◽  
Mesenteric Lymph Nodes ◽  
Cross Sectional ◽  
Mesenteric Lymph ◽  
Swine Herds

ABSTRACT This study investigated the roles of various environmental sources, such as truck-washing systems, waste-processing lagoons, and other sources, as potential contributors to the exposure and dissemination of Salmonella in commercial swine production systems. Four cohorts of nursery age swine herds which originated from distinct farm flows were selected. In addition, cross-sectional sampling of four truck wash stations selected based on the types of disinfectants and sources of water used for sanitizing trucks were tested. Salmonella isolates were recovered from pigs (feces, cecal contents, and mesenteric lymph nodes) and environmental sources (barn floor, lagoon, barn flush, trucks, and holding pens). Antimicrobial susceptibility testing and genotyping were conducted using Kirby-Bauer disk diffusion and amplified fragment length polymorphism, respectively. Salmonella prevalence significantly increased with age from late nursery to slaughter for all of the cohorts (P = 0.007). In two of three instances, all three pig holding pens (lairage) sampled at processing were Salmonella positive. The predominant antibiotypes for all sources included ACSSuT (51.8%), SSuT (16.8%), T (6%), and pansusceptible (7.4%). For the isolates obtained at the farms, the ACSSuT phenotype was 5.6 times more likely to be found in the animals than in the environment (95% confidence interval, 4.4 to 7.2 times). Serogroup B was the most common serogroup (79%), followed by serogroup E (10.4%). Despite the fact that the four production flows were independent, 1 of the 11 genotypic clusters (cluster A1) was commonly detected in any type of sample regardless of its origin. Five of the genotypic clusters (clusters A3, A4, A5, A6, and A7) contained isolates that originated from trucks and lairage swabs and also from cecal contents and/or mesenteric lymph nodes. More interestingly, genotypic clusters A3, A4, and A6 (but not clusters A5 and A7) were not detected on the farms. They originated from the trucks and lairage swabs and then were identified from the cecal contents and/or mesenteric lymph nodes. These findings underscore the significance of various environmental factors, including inadequate truck-washing systems, and emphasize the role of lairage contamination by Salmonella that has food safety significance.

Atrophy of mesenteric lymph nodes in experimental Chagas’ disease: differential role of Fas/Fas-L and TNFRI/TNF pathways

2006 ◽  
Vol 8 (1) ◽  
pp. 221-231 ◽  
Author(s):  
Juliana de Meis ◽  
Daniella Arêas Mendes-da-Cruz ◽  
Désio Aurélio Farias-de-Oliveira ◽  
Eliane Corrêa-de-Santana ◽  
Fernanda Pinto-Mariz ◽  
...  
Keyword(s):  
Lymph Nodes ◽  
Chagas Disease ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Fas L

scholarly journals In situ demonstration of dendritic cell migration from rat intestine to mesenteric lymph nodes: relationships to maturation and role of chemokines

2003 ◽  
Vol 75 (3) ◽  
pp. 434-442 ◽  
Author(s):  
Hisashi Kobayashi ◽  
Soichiro Miura ◽  
Hiroshi Nagata ◽  
Yoshikazu Tsuzuki ◽  
Ryota Hokari ◽  
...  
Keyword(s):  
Cell Migration ◽  
Dendritic Cell ◽  
Lymph Nodes ◽  
Mesenteric Lymph Nodes ◽  
Rat Intestine ◽  
Mesenteric Lymph ◽  
Dendritic Cell Migration

scholarly journals Interleukin (IL)-33 is dispensable for Schistosoma mansoni worm maturation and the maintenance of egg-induced pathology in intestines of infected mice

2020 ◽  
Author(s):  
Jean Pierre Kambala Mukendi ◽  
Risa Nakamura ◽  
Satoshi Uematsu ◽  
Shinjiro Hamano
Keyword(s):  
Lymph Nodes ◽  
Wild Type ◽  
Mesenteric Lymph Nodes ◽  
Schistosome Infection ◽  
Mesenteric Lymph ◽  
Type 2 Immunity ◽  
Transient Impairment ◽  
Inflammatory Infiltrates

Abstract Background: Schistosomes are trematode worms that dwell in their definitive host’s blood vessels, where females lay eggs that need to be discharged into the environment with host excreta to maintain their life cycle. Both worms and eggs require type 2 immunity for their maturation and excretion, respectively. However, immune molecules that orchestrate such immunity remain unclear. IL-33 is one of the epithelium-derived cytokines that induce type 2 immunity in tissues. This study aimed at determining its role in the maturation, reproduction, and excretion of S. mansoni eggs, and in the maintenance of egg-induced pathology in the intestines of mice.Methods: Using S. mansoni-infected IL-33-deficient (IL-33-/-) and wild-type (WT) mice, the morphology of worms and the number of eggs in intestinal tissues were studied at different time points of infection. IL-5 and IL-13 production in spleens and mesenteric lymph nodes were measured. Tissue histology was performed on the terminal ilea of infected and non-infected mice.Results: Morphology-wise, worms from IL-33-/- and WT mice at the fourth and sixth weeks of infection did not differ. The number of eggs in intestinal tissues did not differ much between IL-33-/- and WT mice. In the sixth week of infection, IL-33-/- mice presented impaired type 2 immunity in intestines, characterized by decreased production of IL-5 and IL-13 in mesenteric lymph nodes and fewer inflammatory infiltrates with fewer eosinophils in the ilea. Otherwise there was no difference between IL-33-/- and WT mice in the levels of IL-25 and thymic stromal lymphopoietin (TSLP) in intestinal tissues.Conclusions: Despite its ability to initiate type 2 immunity in tissues, IL-33 alone seems dispensable for S. mansoni maturation and its absence may not affect much the accumulation of eggs in intestinal tissues. The transient impairment of type 2 immunity observed in the intestines, but not spleens, highlights the importance of IL-33 over IL-25 and TSLP in initiating, but not maintaining, locally-induced type 2 immunity in intestinal tissues during schistosome infection. Further studies are needed to decipher the role of each of them in schistosomiasis and clarify the possible interactions that might exist between them.

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