Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

Ampting, Marleen T. J. van; Loonen, L.M.P.; Schonewille, Arjan J.; Konings, Irene; Vink, Carolien; Iovanna, Juan; Chamaillard, Mathias; Dekker, Jan; Meer, Roelof van der; Wells, Jerry M.; Bovee‐Oudenhoven, Ingeborg M. J.

doi:10.1128/iai.06165-11

Cited by 94 publications

(81 citation statements)

References 28 publications

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“…Intestinal AMPPs, immunoglobulins, and a healthy mucus layer are all important factors in the defense against enteric infections (20,(56)(57)(58)(59)(60)(61). CDCA administration, which increased AMPP production, the mucosal B cell fraction, and Muc2 expression, also accelerated the clearance of Citrobacter rodentium infection and limited the systemic spread of Salmonella Typhimurium.…”

Section: Discussionmentioning

confidence: 99%

“…Translocated bacteria are then picked up by mucosal macrophages, transported to mesenteric lymph nodes, and from there spread systemically through the circulation (63). Host defense against Salmonella infection involves Reg3b, Reg3g, and Paneth cell ␣-defensins (20,58,59,64), which are all induced in the ileum by CDCA. It is fair to assume that the combination of higher intestinal AMPP concentrations and a relatively lower number of mucosal macrophages would create a restrictive scenario for the systemic spread of Salmonella.…”

Section: Discussionmentioning

confidence: 99%

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Bile Acid Administration Elicits an Intestinal Antimicrobial Program and Reduces the Bacterial Burden in Two Mouse Models of Enteric Infection

et al. 2017

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In addition to their chemical antimicrobial nature, bile acids are thought to have other functions in the homeostatic control of gastrointestinal immunity. However, those functions have remained largely undefined. In this work, we used ileal explants and mouse models of bile acid administration to investigate the role of bile acids in the regulation of the intestinal antimicrobial response. Mice fed on a diet supplemented with 0.1% chenodeoxycholic acid (CDCA) showed an upregulated expression of Paneth cell ␣-defensins as well as an increased synthesis of the type-C lectins Reg3b and Reg3g by the ileal epithelium. CDCA acted on several epithelial cell types, by a mechanism independent from farnesoid X receptor (FXR) and not involving STAT3 or ␤-catenin activation. CDCA feeding did not change the relative abundance of major commensal bacterial groups of the ileum, as shown by 16S analyses. However, administration of CDCA increased the expression of ileal Muc2 and induced a change in the composition of the mucosal immune cell repertoire, decreasing the proportion of Ly6G ϩ and CD68 ϩ cells, while increasing the relative amount of IgG ϩ B cells. Oral administration of CDCA to mice attenuated infections with the bile-resistant pathogens Salmonella enterica serovar Typhimurium and Citrobacter rodentium, promoting lower systemic colonization and faster bacteria clearance, respectively. Our results demonstrate that bile acid signaling in the ileum triggers an antimicrobial program that can be potentially used as a therapeutic option against intestinal bacterial infections.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Bile Acid Administration Elicits an Intestinal Antimicrobial Program and Reduces the Bacterial Burden in Two Mouse Models of Enteric Infection

et al. 2017

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“…REG receptors are secretory proteins that act on the structure bearing the ligand without modulating the function of their cell of origin (29). Secretory REGs, like 3b and 3g, bind intestinal bacteria and other organisms leading to their demise (30, 31). REG−/− mice show the importance of some of these REGs (30).…”

Section: Mechanisms Of Regulationmentioning

confidence: 99%

Helminth Infections Decrease Host Susceptibility to Immune-Mediated Diseases

Weinstock

Elliott

2014

The Journal of Immunology

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Helminthic infection has become rare in highly industrialized nations. Concurrent with the decline in helminthic infection is an increase in prevalence of inflammatory disease. Removal of helminths from our environment and their powerful effects on host immunity may have contributed to this increase. Several different helminth species can abrogate disease in murine models of inflammatory bowel disease, type 1 diabetes, multiple sclerosis and other conditions. Helminths evoke immune regulatory pathways often involving dendritic cells, Tregs and macrophages that help control disease. Cytokines such as IL4, IL10 and TGFβ have a role. Notable is helminthic modulatory effect on innate immunity, which impedes development of aberrant adaptive immunity. Investigators are identifying key helminth-derived immune modulatory molecules that may have therapeutic utility in the control of inflammatory disease.

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“…A mouse myeloperoxidase (MPO) enzyme-linked immunosorbent assay (ELISA) kit (Hycult Biotechnology, Uden, The Netherlands) was used according to the manufacturer's guidelines to determine the concentration of MPO in intestine mucosal scrapings (39).…”

Section: Methodsmentioning

confidence: 99%

TREM-1 Promotes Survival during Klebsiella pneumoniae Liver Abscess in Mice

Lin

Tseng²,

Yeh

et al. 2014

Infect Immun

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g Klebsiella pneumoniae liver abscess (KPLA) is prevalent in East Asia. Liver abscess can develop after translocation of K. pneumoniae from a patient's bowel into the liver via the portal circulation. TREM-1 (triggering receptor expressed on myeloid cells 1) amplifies inflammatory signaling during infection, but its role in KPLA is poorly understood. We used an animal study to characterize the role of TREM-1 in KPLA. We compared survival rates, bacterial burdens in tissues, inflammatory cytokine levels, and histology findings between wild-type and Trem-1 knockout (KO) mice after oral inoculation of capsular type K1 K. pneumoniae. Translocation of K. pneumoniae to mesenteric lymph nodes and liver was examined, and intestinal permeability, antimicrobial peptide expression, and the clearance of K. pneumoniae in the small intestine were determined. In the absence of TREM-1, KPLA model mice showed increased K. pneumoniae dissemination, enhanced liver and systemic inflammation, and reduced survival. Impaired bacterial clearance in the small intestine causes enhanced K. pneumoniae translocation, which renders Trem-1 KO mice more susceptible to K. pneumoniae oral infection. In conclusion, TREM-1-mediated bacterial clearance in the small intestine is an important immune response against K. pneumoniae. TREM-1 deficiency enhances K. pneumoniae translocation in the small intestine and increases mortality rates in mice with KPLA.

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Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

Cited by 94 publications

References 28 publications

Bile Acid Administration Elicits an Intestinal Antimicrobial Program and Reduces the Bacterial Burden in Two Mouse Models of Enteric Infection

Bile Acid Administration Elicits an Intestinal Antimicrobial Program and Reduces the Bacterial Burden in Two Mouse Models of Enteric Infection

Helminth Infections Decrease Host Susceptibility to Immune-Mediated Diseases

TREM-1 Promotes Survival during Klebsiella pneumoniae Liver Abscess in Mice

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