Distribution of carcinoembryonic antigen‐related cellular adhesion molecules in human gingiva

Huynh-Torlakovic, Hong; Bjerkan, Louise; Schenck, Karl; Blix, Inger J. Schytte

doi:10.1111/j.1600-0722.2012.00981.x

Cited by 6 publications

(4 citation statements)

References 32 publications

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“…It will be also important to take into account that an up-regulation of CEACAMs might be transient either due to temporary qualities of chronic/persistent disease or due to pathogen characteristics at distinct time points during the infection process. It will also be interesting to test human lung tissues for the presence of the other CEACAMs expressed on epithelial cells (CEACAM7, 18, 20 and 21 [56,57]) and to analyze their ability to interact with pathogens.…”

Section: Discussionmentioning

confidence: 99%

Carcinoembryonic antigen (CEA)-related cell adhesion molecules are co-expressed in the human lung and their expression can be modulated in bronchial epithelial cells by non-typable Haemophilus influenzae, Moraxella catarrhalis, TLR3, and type I and II interferons

et al. 2013

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BackgroundThe carcinoembryonic antigen (CEA)-related cell adhesion molecules CEACAM1 (BGP, CD66a), CEACAM5 (CEA, CD66e) and CEACAM6 (NCA, CD66c) are expressed in human lung. They play a role in innate and adaptive immunity and are targets for various bacterial and viral adhesins. Two pathogens that colonize the normally sterile lower respiratory tract in patients with chronic obstructive pulmonary disease (COPD) are non-typable Haemophilus influenzae (NTHI) and Moraxella catarrhalis. Both pathogens bind to CEACAMs and elicit a variety of cellular reactions, including bacterial internalization, cell adhesion and apoptosis.MethodsTo analyze the (co-) expression of CEACAM1, CEACAM5 and CEACAM6 in different lung tissues with respect to COPD, smoking status and granulocyte infiltration, immunohistochemically stained paraffin sections of 19 donors were studied. To address short-term effects of cigarette smoke and acute inflammation, transcriptional regulation of CEACAM5, CEACAM6 and different CEACAM1 isoforms by cigarette smoke extract, interferons, Toll-like receptor agonists, and bacteria was tested in normal human bronchial epithelial (NHBE) cells by quantitative PCR. Corresponding CEACAM protein levels were determined by flow cytometry.ResultsImmunohistochemical analysis of lung sections showed the most frequent and intense staining for CEACAM1, CEACAM5 and CEACAM6 in bronchial and alveolar epithelium, but revealed no significant differences in connection with COPD, smoking status and granulocyte infiltration. In NHBE cells, mRNA expression of CEACAM1 isoforms CEACAM1-4L, CEACAM1-4S, CEACAM1-3L and CEACAM1-3S were up-regulated by interferons alpha, beta and gamma, as well as the TLR3 agonist polyinosinic:polycytidylic acid (poly I:C). Interferon-gamma also increased CEACAM5 expression. These results were confirmed on protein level by FACS analysis. Importantly, also NTHI and M. catarrhalis increased CEACAM1 mRNA levels. This effect was independent of the ability to bind to CEACAM1. The expression of CEACAM6 was not affected by any treatment or bacterial infection.ConclusionsWhile we did not find a direct correlation between CEACAM1 expression and COPD, the COPD-associated bacteria NTHi and M. catarrhalis were able to increase the expression of their own receptor on host cells. Further, the data suggest a role for CEACAM1 and CEACAM5 in the phenomenon of increased host susceptibility to bacterial infection upon viral challenge in the human respiratory tract.

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Section: Discussionmentioning

confidence: 99%

Carcinoembryonic antigen (CEA)-related cell adhesion molecules are co-expressed in the human lung and their expression can be modulated in bronchial epithelial cells by non-typable Haemophilus influenzae, Moraxella catarrhalis, TLR3, and type I and II interferons

et al. 2013

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“…Since increased receptor density demonstrably increases the chances of cellular invasion by bacteria [26], these observations suggest that CEACAMs may play a critical role in mucosal colonisation and pathogenesis. CEACAM1, CEA, and CEACAM6 are expressed in human junctional epithelium [27]. However, whether other ororespiratory bacterial colonisers/pathogens besides Nm, Hi, and Mx target CEACAMs has not been fully investigated.…”

Section: Introductionmentioning

confidence: 99%

Fusobacterium spp. target human CEACAM1 via the trimeric autotransporter adhesin CbpF

Brewer

Dymock

Brady

et al. 2019

Journal of Oral Microbiology

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Neisseria meningitidis, Haemophilus influenzae, and Moraxella catarrhalis are pathogenic bacteria adapted to reside on human respiratory mucosal epithelia. One common feature of these species is their ability to target members of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family, especially CEACAM1, which is achieved via structurally distinct ligands expressed by each species. Beside respiratory epithelial cells, cells at the dentogingival junction express high levels of CEACAM1. It is possible that bacterial species resident within the oral cavity also utilise CEACAM1 for colonisation and invasion of gingival tissues. From a screen of 59 isolates from the human oral cavity representing 49 bacterial species, we identified strains from Fusobacterium bound to CEACAM1. Of the Fusobacterium species tested, the CEACAM1-binding property was exhibited by F. nucleatum (Fn) and F. vincentii (Fv) but not F. polymorphum (Fp) or F. animalis (Fa) strains tested. These studies identified that CEACAM adhesion was mediated using a trimeric autotransporter adhesin (TAA) for which no function has thus far been defined. We therefore propose the name CEACAM binding protein of Fusobacterium (CbpF). CbpF was identified to be present in the majority of unspeciated Fusobacterium isolates confirming a subset of Fusobacterium spp. are able to target human CEACAM1.

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“…However, the ceacam1 gene is highly upregulated during palate development [ 88 ]. Moreover, CEACAM expression in the oral cavity is upregulated in patients with oral cancer, periodontitis, and oral lichen planus, as well as in smokers [ 89 , 90 , 91 , 92 ]. Therefore, in some pathological conditions, the increased expression of oral CEACAMs may favor H. pylori adhesion to oral host cells and even create favorable conditions for CagA injection into oral cells, inducing inflammatory factors.…”

Section: Interactions Between H Pylori and Microen...mentioning

confidence: 99%

Helicobacter pylori in the Oral Cavity: Current Evidence and Potential Survival Strategies

Zhang

Chen

Ren

et al. 2022

IJMS

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Helicobacter pylori (H. pylori) is transmitted primarily through the oral–oral route and fecal–oral route. The oral cavity had therefore been hypothesized as an extragastric reservoir of H. pylori, owing to the presence of H. pylori DNA and particular antigens in distinct niches of the oral cavity. This bacterium in the oral cavity may contribute to the progression of periodontitis and is associated with a variety of oral diseases, gastric eradication failure, and reinfection. However, the conditions in the oral cavity do not appear to be ideal for H. pylori survival, and little is known about its biological function in the oral cavity. It is critical to clarify the survival strategies of H. pylori to better comprehend the role and function of this bacterium in the oral cavity. In this review, we attempt to analyze the evidence indicating the existence of living oral H. pylori, as well as potential survival strategies, including the formation of a favorable microenvironment, the interaction between H. pylori and oral microorganisms, and the transition to a non-growing state. Further research on oral H. pylori is necessary to develop improved therapies for the prevention and treatment of H. pylori infection.

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Distribution of carcinoembryonic antigen‐related cellular adhesion molecules in human gingiva

Cited by 6 publications

References 32 publications

Carcinoembryonic antigen (CEA)-related cell adhesion molecules are co-expressed in the human lung and their expression can be modulated in bronchial epithelial cells by non-typable Haemophilus influenzae, Moraxella catarrhalis, TLR3, and type I and II interferons

Carcinoembryonic antigen (CEA)-related cell adhesion molecules are co-expressed in the human lung and their expression can be modulated in bronchial epithelial cells by non-typable Haemophilus influenzae, Moraxella catarrhalis, TLR3, and type I and II interferons

Fusobacterium spp. target human CEACAM1 via the trimeric autotransporter adhesin CbpF

Helicobacter pylori in the Oral Cavity: Current Evidence and Potential Survival Strategies

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