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Mucosal Immunology

Kara J Filbey, Mali Camberis, Jodie Chandler, Rufus Turner, Anthony J Kettle, Ramon M Eichenberger, Paul Giacomin, Graham Le Gros
The ability of helminths to manipulate the immune system of their hosts to ensure their own survival is often credited with affecting responses to other pathogens. We undertook co-infection experiments in mice to determine how infection with the intestinal helminth Heligmosomoides polygyrus affected the parasitological, immunological and physiological outcomes of a primary infection with a distinct species of helminth; the lung migratory parasite Nippostrongylus brasiliensis. We found that migrating N. brasiliensis larvae were killed in the lungs of H...
November 6, 2018: Mucosal Immunology
P J Sarate, S Heinl, S Poiret, M Drinić, C Zwicker, I Schabussova, C Daniel, U Wiedermann
Following the publication of this article, the authors have requested that the Acknowledgements section be amended to include the financing source of the study. The correct Acknowledgments should be as follows: We gratefully acknowledge funding from the Austrian Science Fund SFB F46 and DK MCCA W1248-B30, OeAD-GmbH grants (FR13/2016) and from the Amadeus partnership Hubert Curein French and Austrian program. We thank the BioImaging Center of Lille (Frank Lafont) for the use of the IVIS Lumina XR. We gratefully thank Katharina Ambroz, Elke Korb, Karin Baier, Erika Garner-Spitzer, Joshua Tobias, Gwenaëlle Verbrugghe, and Jéremy Desramaut for their technical assistance and helpful discussions...
November 1, 2018: Mucosal Immunology
J S Lin, K Mohrs, F M Szaba, L W Kummer, E A Leadbetter, M Mohrs
Epidemiological data and animal studies suggest that helminth infection exerts potent immunomodulatory effects that dampen host immunity against unrelated pathogens. Despite this notion, we unexpectedly discovered that prior helminth infection resulted in enhanced protection against subsequent systemic and enteric bacterial infection. A population of virtual memory CD8 T (CD8 TVM ) cells underwent marked expansion upon infection with the helminth Heligmosomoides polygurus by an IL-4-regulated, antigen-independent mechanism...
October 25, 2018: Mucosal Immunology
Yingzi Cong, Yanqing Li
No abstract text is available yet for this article.
October 25, 2018: Mucosal Immunology
Jeanie Quach, France Moreau, Christina Sandall, Kris Chadee
During invasion, Entamoeba histolytica (Eh) encounter macrophages and activate them to elicit tissue damaging pro-inflammatory responses. When Eh binds macrophages via the Gal-lectin, surface EhCP-A5 RGD sequence ligates α5 β1 integrin to activate caspase-1 in a complex known as the NLRP3 inflammasome. In this study, we investigated Eh requirements underlying macrophage caspase-4 and -1 activation and the role caspase-4 and gasdermin D (GSDMD) play in augmenting pro-inflammatory cytokine responses. Caspase-4 activation was similar to caspase-1 requiring live Eh attachment via the Gal-lectin and EhCP-A5...
October 25, 2018: Mucosal Immunology
N Garrido-Mesa, J-H Schroeder, E Stolarczyk, A L Gallagher, J W Lo, C Bailey, L Campbell, V Sexl, T T MacDonald, J K Howard, R K Grencis, N Powell, G M Lord
Innate lymphoid cells (ILCs) play an important role in regulating immune responses at mucosal surfaces. The transcription factor T-bet is crucial for the function of ILC1s and NCR+ ILC3s and constitutive deletion of T-bet prevents the development of these subsets. Lack of T-bet in the absence of an adaptive immune system causes microbiota-dependent colitis to occur due to aberrant ILC3 responses. Thus, T-bet expression in the innate immune system has been considered to dampen pathogenic immune responses. Here, we show that T-bet plays an unexpected role in negatively regulating innate type 2 responses, in the context of an otherwise intact immune system...
October 24, 2018: Mucosal Immunology
Li-Yin Hung, Debasish Sen, Taylor K Oniskey, Jeremey Katzen, Noam A Cohen, Andrew E Vaughan, Wildaliz Nieves, Anatoly Urisman, Michael F Beers, Matthew F Krummel, De'Broski R Herbert
Coordinated efforts between macrophages and epithelia are considered essential for wound healing, but the macrophage-derived molecules responsible for repair are poorly defined. This work demonstrates that lung macrophages rely upon Trefoil factor 2 to promote epithelial proliferation following damage caused by sterile wounding, Nippostrongylus brasiliensis or Bleomycin sulfate. Unexpectedly, the presence of T, B, or ILC populations was not essential for macrophage-driven repair. Instead, conditional deletion of TFF2 in myeloid-restricted CD11cCre TFF2 flox mice exacerbated lung pathology and reduced the proliferative expansion of CD45- EpCAM+ pro-SPC+ alveolar type 2 cells...
October 18, 2018: Mucosal Immunology
Bruno Galvão-Filho, Júlia Teixeira de Castro, Maria Marta Figueiredo, Claudio Gonçalves Rosmaninho, Lis Ribeiro do Valle Antonelli, Ricardo Tostes Gazzinelli
Malaria-associated acute respiratory distress syndrome (MA-ARDS) and acute lung injury (ALI) are complications that cause lung damage and often leads to death. The MA-ARDS/ALI is associated with a Type 1 inflammatory response mediated by T lymphocytes and IFN-γ. Here, we used the Plasmodium berghei NK65 (PbN)-induced MA-ALI/ARDS model that resembles human disease and confirmed that lung CD4+ and CD8+ T cells predominantly expressed Tbet and IFN-γ. Surprisingly, we found that development of MA-ALI/ARDS was dependent on functional CCR4, known to mediate the recruitment of Th2 lymphocytes and regulatory T cells...
October 18, 2018: Mucosal Immunology
Kari Ann Shirey, Mary E Sunday, Wendy Lai, Mira C Patel, Jorge C G Blanco, Frank Cuttitta, Stefanie N Vogel
Gastrin-releasing peptide (GRP) is an evolutionarily well-conserved neuropeptide that was originally recognized for its ability to mediate gastric acid secretion in the gut. More recently, however, GRP has been implicated in pulmonary lung inflammatory diseases including bronchopulmonary dysplasia, chronic obstructive pulmonary disease, emphysema, and others. Antagonizing GRP or its receptor mitigated lethality associated with the onset of viral pneumonia in a well-characterized mouse model of influenza. In mice treated therapeutically with the small-molecule GRP inhibitor, NSC77427, increased survival was accompanied by decreased numbers of GRP-producing pulmonary neuroendocrine cells, improved lung histopathology, and suppressed cytokine gene expression...
October 16, 2018: Mucosal Immunology
Samira Mansouri, Seema Patel, Divya S Katikaneni, Steven M Blaauboer, Wei Wang, Stefan Schattgen, Katherine Fitzgerald, Lei Jin
Cyclic dinucleotides (CDNs), including cyclic di-GMP (CDG), are promising vaccine adjuvants in preclinical/clinical trials. The in vivo mechanisms of CDNs are not clear. Here we investigated the roles of lung DC subsets in promoting CDG mucosal adjuvant responses in vivo. Using genetically modified mice and adoptive cell transfer, we identified lung conventional DC 2 (cDC2) as the central player in CDG mucosal responses. We further identified two functionally distinct lung cDC2 subpopulations: TNFR2+ pRelB+ and TNFR2- pRelB- cDC2...
October 16, 2018: Mucosal Immunology
Bibiana E Barrios, Lisa Maccio-Maretto, F Nicolás Nazar, Silvia G Correa
Biological rhythms are periodic oscillations that occur in the physiology of the organism and the cells. The rhythms of the immune system are strictly regulated and the circadian alteration seems to have serious consequences. Even so, it is not clear how the immune cells of the intestinal mucosa synchronize with the external environment. Besides, little is known about the way in which biological rhythms affect the critical functions of intestinal immunity, such as oral tolerance. We studied fluctuations in the relevant parameters of intestinal immunity at four different times throughout the day...
October 16, 2018: Mucosal Immunology
Megan R Sanctuary, Rick H Huang, Ashleigh A Jones, Marisa E Luck, Carol M Aherne, Paul Jedlicka, Edwin F de Zoeten, Colm B Collins
Pro-inflammatory cytokine TNFα antagonizes regulatory T cell (Treg) suppressive function with a measurable reduction of IL-10 protein secretion. Tregs are critical to suppress excessive immune activation, particularly within the intestine where high antigenic loads elicit chronic subclinical immune activation. Employing a TNFα-driven murine inflammatory bowel disease (IBD) model (TNFΔARE/+ ), which mirrors the Treg expansion and transmural ileitis seen in Crohn's disease, we demonstrate that the TNFα-mediated loss of Treg suppressive function coincides with induction of a specific miRNA, miR-106a in both humans and mice, via NFκB promoter binding to suppress post-transcriptional regulation of IL-10 release...
October 16, 2018: Mucosal Immunology
Eveline Bennek, Ana D Mandić, Julien Verdier, Silvia Roubrocks, Oliver Pabst, Niels Van Best, Inga Benz, Thomas Kufer, Christian Trautwein, Gernot Sellge
Oral tolerance to soluble antigens is critically important for the maintenance of immunological homeostasis in the gut. The mechanisms of tolerance induction to antigens of the gut microbiota are still less well understood. Here, we investigate whether the subcellular localization of antigens within non-pathogenic E. coli has a role for its ability to induce antigen-specific tolerance. E. coli that express an ovalbumin (OVA) peptide in the cytoplasm, at the outer membrane or as secreted protein were generated...
October 16, 2018: Mucosal Immunology
David M Habiel, Milena S Espindola, Chris Kitson, Anthony V Azzara, Ana Lucia Coelho, Barry Stripp, Cory M Hogaboam
Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung disease, with unknown etiopathogenesis and suboptimal therapeutic options. Previous reports have shown that increased T-cell numbers and CD28null phenotype is predictive of prognosis in IPF, suggesting that these cells might have a role in this disease. Flow cytometric analysis of explanted lung cellular suspensions showed a significant increase in CD8+ CD28null T cells in IPF relative to normal lung explants. Transcriptomic analysis of CD3+ T cells isolated from IPF lung explants revealed a loss of CD28-transcript expression and elevation of pro-inflammatory cytokine expression in IPF relative to normal T cells...
October 12, 2018: Mucosal Immunology
June L Chan, Shaoguang Wu, Abby L Geis, Gabrielle V Chan, Talles A M Gomes, Sarah E Beck, Xinqun Wu, Hongni Fan, Ada J Tam, Liam Chung, Hua Ding, Hao Wang, Drew M Pardoll, Franck Housseau, Cynthia L Sears
Polysaccharide A (PSA), an immunogenic capsular component of non-toxigenic Bacteroides fragilis (NTBF) strain NCTC 9343, is reported to promote mucosal immune development and suppress colitis. Contrastingly, enterotoxigenic Bacteroides fragilis (ETBF) is highly associated with inflammatory bowel disease (IBD) and colorectal cancer (CRC), rapidly inducing IL-17-dependent murine colitis and tumorigenesis. In specific-pathogen-free (SPF) C57BL/6 wild-type (WT) and multiple intestinal neoplasia (MinApc716+/- ) mice, we show that sequential treatment of the NTBF strain, 9343, followed by the ETBF strain, 86-5443-2-2 (86), diminished colitis and tumorigenesis...
October 2, 2018: Mucosal Immunology
Dulce C Macias-Ceja, Dolores Ortiz-Masiá, Pedro Salvador, Laura Gisbert-Ferrándiz, Carlos Hernández, Martin Hausmann, Gerhard Rogler, Juan V Esplugues, Joaquín Hinojosa, Rafael Alós, Francisco Navarro, Jesus Cosin-Roger, Sara Calatayud, María D Barrachina
Succinate, an intermediate of the tricarboxylic acid cycle, is accumulated in inflamed areas and its signaling through succinate receptor (SUCNR1) regulates immune function. We analyze SUCNR1 expression in the intestine of Crohn's disease patients and its role in murine intestinal inflammation and fibrosis. We show that both serum and intestinal succinate levels and SUCNR1 expression in intestinal surgical resections were higher in CD patients than in controls. SUCNR1 co-localized with CD86, CD206, and α-SMA+ cells in human intestine and we found a positive and significant correlation between SUCNR1 and α-SMA expression...
October 2, 2018: Mucosal Immunology
Nesrine Makhezer, Marwa Ben Khemis, Dan Liu, Yamina Khichane, Viviana Marzaioli, Asma Tlili, Marjan Mojallali, Coralie Pintard, Philippe Letteron, Margarita Hurtado-Nedelec, Jamel El-Benna, Jean-Claude Marie, Aurélie Sannier, Anne-Laure Pelletier, Pham My-Chan Dang
Inflammatory bowel disease (IBD) is characterized by severe and recurrent inflammation of the gastrointestinal tract, associated with altered patterns of cytokine synthesis, excessive reactive oxygen species (ROS) production, and high levels of the innate immune protein, lipocalin-2 (LCN-2), in the mucosa. The major source of ROS in intestinal epithelial cells is the NADPH oxidase NOX1, which consists of the transmembrane proteins, NOX1 and p22PHOX , and the cytosolic proteins, NOXO1, NOXA1, and Rac1. Here, we investigated whether NOX1 activation and ROS production induced by key inflammatory cytokines in IBD causally affects LCN-2 production in colonic epithelial cells...
October 2, 2018: Mucosal Immunology
T G Moreira, L S Horta, A C Gomes-Santos, R P Oliveira, N M G P Queiroz, D Mangani, B Daniel, A T Vieira, S Liu, A M Rodrigues, D A Gomes, G Gabriely, E Ferreira, H L Weiner, R M Rezende, L Nagy, A M C Faria
Conjugated linoleic acid (CLA) has been shown to activate the nuclear receptor PPAR-γ and modulate metabolic and immune functions. Despite the worldwide use of CLA dietary supplementation, strong scientific evidence for its proposed beneficial actions are missing. We found that CLA-supplemented diet reduced mucosal damage and inflammatory infiltrate in the dextran sodium sulfate (DSS)-induced colitis model. Conditional deletion of PPAR-γ in macrophages from mice supplemented with CLA diet resulted in loss of this protective effect of CLA, suggesting a PPAR-γ-dependent mechanism mediated by macrophages...
October 2, 2018: Mucosal Immunology
Sagar Paudel, Laxman Ghimire, Liliang Jin, Pankaj Baral, Shanshan Cai, Samithamby Jeyaseelan
Gram-positive pathogens, including Staphylococcus aureus, cause necrotizing pneumonia. The central feature of S. aureus pneumonia is toxin-induced necroptosis of immune and resident cells, which impedes host defense. However, the role of the NLRC4 in the lung following S. aureus infection remains elusive. Here, we demonstrate that S. aureus activates the NLRC4 to drive necroptosis and IL-18 production, which impaired IL-17A-dependent neutrophil-mediated host susceptibility. In particular, Nlrc4-/- mice exhibit reduced necroptosis, enhanced neutrophil influx into the lungs, decreased bacterial burden, and improved host survival...
October 2, 2018: Mucosal Immunology
Daniel R Saban, Robin R Hodges, Rose Mathew, Nancy J Reyes, Chen Yu, Rebecca Kaye, William Swift, Nora Botten, Charles N Serhan, Darlene A Dartt
Severe, chronic eye allergy is an understudied, vision-threatening condition. Treatments remain limited. We used a mouse model of severe allergic eye disease (AED) to determine whether topical application of the pro-resolution mediator Resolvin D1 (RvD1) terminates the response. AED was induced by injection of ovalbumin (OVA) followed by topical challenge of OVA daily. RvD1 was applied topically prior to OVA. Clinical symptoms were scored. Eye washes were assayed for MUC5AC. After 7 days, eyes were removed and the number of goblet cells, T helper cell responses and presence of immune cells in draining lymph nodes and conjunctiva determined...
October 2, 2018: Mucosal Immunology
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