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Epithelium-Immune Cell Interactions Underlying Innate and Adaptive Immunity

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 12505

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Prof. Dr. Scott M. O'Grady

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Guest Editor

Department of Animal Science, College of Food, Agricultural and Natural Resource Sciences, University of Minnesota, St. Paul, MN 55108, USA
Interests: membrane transport; epithelial ion transport; ion channels and transporters; ionotropic receptors; purinergic signaling; role of epithelial cells in innate immunity

Special Issue Information

Dear Colleagues,

Epithelial cells located in various organs play an essential role in coordinating immune responses to danger signals released in response to pathogen invasion or tissue damage. Although they are not professional immune cells, they are an essential component of the immune response to infection. In settings where chronic inflammation contributes significantly to disease pathology, epithelial cells function as regulators of innate and adaptive immunity by secreting signaling molecules or by expressing antigens on their cell membranes that can dramatically alter the function of immune cells and shape the inflammatory response. Furthermore, epithelial cells release a variety of defense molecules that act directly to kill invading microbes. Structurally, epithelial cells maintain tight junctions that serve as a barrier to prevent pathogen and antigen access to the submucosa, which typically exacerbates inflammation. The epithelium also initiates adaptive immune responses by modulating both activation and differentiation of dendritic cells, B cells, and T cells. While our understanding of epithelial regulation of innate and adaptive immunity has advanced, more research is needed in order to identify additional molecular mechanisms as potential targets for development of pharmaceuticals that can control inflammation.

Therefore, in this Special Issue, primary research papers and review articles related to the topic of epithelium-immune cell interactions underlying innate and adaptive immunity are invited.

Prof. Dr. Scott M. O'Grady
Guest Editor

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Keywords

Cytokines
Chemokines
Defensins
Inflammation
Alarmins
Type 2 immunity
Damage-associated molecular patterns (DAMPs)
Pathogen-associated molecular patterns (PAMPs)

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Published Papers (4 papers)

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Research

21 pages, 10300 KiB

Open AccessArticle

Immunohistochemical Expression Pattern of FGFR1, FGFR2, RIP5, and HIP2 in Developing and Postnatal Kidneys of Dab1^−/− (yotari) Mice

by Nela Kelam, Anita Racetin, Yu Katsuyama, Katarina Vukojević and Sandra Kostić

Int. J. Mol. Sci. 2022, 23(4), 2025; https://doi.org/10.3390/ijms23042025 - 11 Feb 2022

Cited by 5 | Viewed by 2282

Abstract

This study aimed to explore how Dab1 gene functional silencing influences the spatial and temporal expression patterns of fibroblast growth factor receptor 1 (FGFR1), fibroblast growth factor receptor 2 (FGFR2), receptor-interacting protein kinase 5 (RIP5), and huntingtin-interacting protein 2 (HIP2) in the developing and postnatal kidneys of the yotari mice as potential determinants of normal kidney formation and function. Dab1^−/− animal kidneys exhibit diminished FGFR1/FGFR2 expression in all examined developmental stages, whereas RIP5 cell immunoreactivity demonstrated negligible variation. The HIP2 expression revealed a discernible difference during the postnatal period, where we noted a significant decrease in almost all the observed kidney structures of yotari animals. An extracellular signal-regulated kinase (Erk1/2) and mammalian target of rapamycin (mTOR) expression in yotari kidneys decreased in embryonic and postnatal developmental phases for which we can hypothesize that the Erk1/2 signaling pathway in the yotari mice kidneys is dependent on Reelin with Dab1 only partially implicated in Reelin-mediated MEK/Erk1/2 activation. The impairment of FGFR1 and FGFR2 expression suggests the involvement of the observed markers in generating the CAKUT phenotype resulting in renal hypoplasia. Our study demonstrates the critical role of HIP2 in reducing cell death throughout nephrogenesis and maturation in wild-type mice and indicates a possible connection between decreased HIP2 expression in postnatal kidney structures and observed podocyte injury in yotari. Our results emphasize the crucial function of the examined markers throughout normal kidney development and their potential participation in kidney pathology and diagnostics, where they might serve as biomarkers and therapeutic targets. Full article

(This article belongs to the Special Issue Epithelium-Immune Cell Interactions Underlying Innate and Adaptive Immunity)

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18 pages, 2837 KiB

Open AccessArticle

Airway Exposure to Polyethyleneimine Nanoparticles Induces Type 2 Immunity by a Mechanism Involving Oxidative Stress and ATP Release

by Yotesawee Srisomboon, Noriyuki Ohkura, Koji Iijima, Takao Kobayashi, Peter J. Maniak, Hirohito Kita and Scott M. O’Grady

Int. J. Mol. Sci. 2021, 22(16), 9071; https://doi.org/10.3390/ijms22169071 - 23 Aug 2021

Cited by 13 | Viewed by 2699

Abstract

Polyethyleneimine (PEI) induced immune responses were investigated in human bronchial epithelial (hBE) cells and mice. PEI rapidly induced ATP release from hBE cells and pretreatment with glutathione (GSH) blocked the response. PEI activated two conductive pathways, VDAC-1 and pannexin 1, which completely accounted for ATP efflux across the plasma membrane. Moreover, PEI increased intracellular Ca²⁺ concentration ([Ca²⁺]_i), which was reduced by the pannexin 1 inhibitor, ¹⁰Panx (50 μM), the VDAC-1 inhibitor, DIDS (100 μM), and was nearly abolished by pretreatment with GSH (5 mM). The increase in [Ca²⁺]_i involved Ca²⁺ uptake through two pathways, one blocked by oxidized ATP (oATP, 300 μM) and another that was blocked by the TRPV-1 antagonist A784168 (100 nM). PEI stimulation also increased IL-33 mRNA expression and protein secretion. In vivo experiments showed that acute (4.5 h) PEI exposure stimulated secretion of Th2 cytokines (IL-5 and IL-13) into bronchoalveolar lavage (BAL) fluid. Conjugation of PEI with ovalbumin also induced eosinophil recruitment and secretion of IL-5 and IL-13 into BAL fluid, which was inhibited in IL-33 receptor (ST2) deficient mice. In conclusion, PEI-induced oxidative stress stimulated type 2 immune responses by activating ATP-dependent Ca²⁺ uptake leading to IL-33 secretion, similar to allergens derived from Alternaria. Full article

(This article belongs to the Special Issue Epithelium-Immune Cell Interactions Underlying Innate and Adaptive Immunity)

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18 pages, 3285 KiB

Open AccessArticle

The CXCL2/IL8/CXCR2 Pathway Is Relevant for Brain Tumor Malignancy and Endothelial Cell Function

by Ruth M. Urbantat, Anne Blank, Irina Kremenetskaia, Peter Vajkoczy, Güliz Acker and Susan Brandenburg

Int. J. Mol. Sci. 2021, 22(5), 2634; https://doi.org/10.3390/ijms22052634 - 5 Mar 2021

Cited by 30 | Viewed by 4249

Abstract

We aimed to evaluate the angiogenic capacity of CXCL2 and IL8 affecting human endothelial cells to clarify their potential role in glioblastoma (GBM) angiogenesis. Human GBM samples and controls were stained for proangiogenic factors. Survival curves and molecule correlations were obtained from the TCGA (The Cancer Genome Atlas) database. Moreover, proliferative, migratory and angiogenic activity of peripheral (HUVEC) and brain specific (HBMEC) primary human endothelial cells were investigated including blockage of CXCR2 signaling with SB225502. Gene expression analyses of angiogenic molecules from endothelial cells were performed. Overexpression of VEGF and CXCL2 was observed in GBM patients and associated with a survival disadvantage. Molecules of the VEGF pathway correlated but no relation for CXCR1/2 and CXCL2/IL8 was found. Interestingly, receptors of endothelial cells were not induced by addition of proangiogenic factors in vitro. Proliferation and migration of HUVEC were increased by VEGF, CXCL2 as well as IL8. Their sprouting was enhanced through VEGF and CXCL2, while IL8 showed no effect. In contrast, brain endothelial cells reacted to all proangiogenic molecules. Additionally, treatment with a CXCR2 antagonist led to reduced chemokinesis and sprouting of endothelial cells. We demonstrate the impact of CXCR2 signaling on endothelial cells supporting an impact of this pathway in angiogenesis of glioblastoma. Full article

(This article belongs to the Special Issue Epithelium-Immune Cell Interactions Underlying Innate and Adaptive Immunity)

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15 pages, 3239 KiB

Open AccessCommunication

High-Fat Diet and Age-Dependent Effects of IgA-Bearing Cell Populations in the Small Intestinal Lamina Propria in Mice

by Yuta Sakamoto, Masatoshi Niwa, Ken Muramatsu and Satoshi Shimo

Int. J. Mol. Sci. 2021, 22(3), 1165; https://doi.org/10.3390/ijms22031165 - 25 Jan 2021

Cited by 5 | Viewed by 2473

Abstract

Several studies highlighted that obesity and diabetes reduce immune function. However, changes in the distribution of immunoglobins (Igs), including immunoglobulin-A (IgA), that have an important function in mucosal immunity in the intestinal tract, are unclear. This study aimed to investigate the impaired immune functions in the context of a diet-induced obese murine model via the assessment of the Igs in the intestinal villi. We used mice fed a high-fat diet (HFD) from four to 12 or 20 weeks of age. The distributions of IgA, IgM, and IgG1 were observed by immunohistochemistry. Interestingly, we observed that IgA was immunolocalized in many cells of the lamina propria and that immunopositive cells increased in mice aged 12 to 20 weeks. Notably, mice fed HFD showed a reduced number of IgA-immunopositive cells in the intestinal villi compared to those fed standard chow. Of note, the levels of IgM and IgG1 were also reduced in HFD fed mice. These results provide insights into the impaired mucosal immune function arising from diet-induced obesity and type 2 diabetes. Full article

(This article belongs to the Special Issue Epithelium-Immune Cell Interactions Underlying Innate and Adaptive Immunity)

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