Submitted Successfully!
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Ver. Summary Created by Modification Content Size Created at Operation
1 -- 2371 2022-12-08 02:13:25 |
2 update references and layout -18 word(s) 2353 2022-12-08 03:48:20 |

Video Upload Options

Do you have a full video?


Are you sure to Delete?
If you have any further questions, please contact Encyclopedia Editorial Office.
Kim, S.;  Cho, K. Extracellular Vesicles in Allergic Airway Disease. Encyclopedia. Available online: (accessed on 05 December 2023).
Kim S,  Cho K. Extracellular Vesicles in Allergic Airway Disease. Encyclopedia. Available at: Accessed December 05, 2023.
Kim, Sung-Dong, Kyu-Sup Cho. "Extracellular Vesicles in Allergic Airway Disease" Encyclopedia, (accessed December 05, 2023).
Kim, S., & Cho, K.(2022, December 08). Extracellular Vesicles in Allergic Airway Disease. In Encyclopedia.
Kim, Sung-Dong and Kyu-Sup Cho. "Extracellular Vesicles in Allergic Airway Disease." Encyclopedia. Web. 08 December, 2022.
Extracellular Vesicles in Allergic Airway Disease

Mesenchymal stem cells (MSCs) have been reported as promising candidates for the treatment of various diseases, especially allergic diseases, as they have the capacity to differentiate into various cells. MSCs itself has several limitations such as risk of aneuploidy, difficulty in handling, immune rejection, tumorigenicity, so interest in the extracellular vesicles (EVs) released from MSCs is increasing and many studies have been reported. Previous studies have shown that extracellular vesicles (EVs) produced by MSCs is as effective as the MSCs themselves in suppression of allergic airway inflammation through the suppression of Th2 cytokine production and induction of regulatory T cells (Treg) expansion. EVs is one of the substances secreted by paracrine induction from MSCs, and because it exerts its effect by delivering contents such as mRNA, microRNA, and protein to the receptor cell, it can reduce the problems or risks related to stem cell therapy.

mesenchymal stem cells extracellular vesicles asthma allergic rhinitis

1. Introduction

Allergic rhinitis and asthma are representative atopic diseases, and 30% of allergic rhinitis patients have asthma and 70% of asthma patients have allergic rhinitis [1][2]. Allergic rhinitis and asthma are caused by various antigens and specific immunoglobulin E (Ig E), and they are immunologically characterized by the excessive activation of type 2 helper T (Th2) cells [3]. Th2 cell-induced inflammation is characterized by a significant increase in interleukin (IL)-4, IL-5, and IL-13 levels, which induce and high serum Ig E levels and airway eosinophilic inflammation and airway hyper responsiveness (AHR) [3]. The Th1 and Th2 cytokines are mutually antagonistic, and the selective suppression of Th2 responses may be crucial for protection against allergic inflammation [1][3]. There is mounting evidence that the insufficient suppression of Tregs as well as the imbalance of Th1/Th2 responses in the pathogenesis of allergic airway disease play an important role in excessive Th2 responses [4].
Stem cells are undifferentiated cells that have the potential to develop into many different cell types. They have been reported to possess the ability to self-renew in an undifferentiated state and to differentiate into many types of cells with specific functions upon receiving appropriate triggers. Stem cells can be divided into two groups, embryonic and adult. Embryonic stem cells are derived during early development at the blastocyst stage, and they are pluripotent, implying they can develop into any cell type. However, adult stem cells are multipotent, meaning they can only differentiate into certain types of tissue [5]. Both embryonic and adult stem cells have been studied as a promising source for therapeutic applications in the repair of damaged tissues and regenerative medicine [6][7][8][9].
Mesenchymal stem cells (MSCs) represent an important stem cell population with multi-potent capabilities, which means that they may have high utility for translational clinical applications. MSCs can be isolated from a number of adult tissues, and they can differentiate into several mesenchymal lineages both in vitro and in vivo, such as adipose tissue, cartilage, bone, muscle, and nerve [10][11][12][13][14].
In addition to their multi-lineage potential, MSCs have been shown to possess the unique ability to suppress an immune response and modulate inflammation. MSCs can inhibit natural killer cell functions, modulate dendritic cell maturation, and suppress the allogeneic T cell response by alternating the cytokine secretion profile of dendritic cells and T cells induced by an allogeneic immune reaction [15][16]. Therefore, MSCs have been reported to have anti-inflammatory and immunomodulatory effects in various chronic inflammatory diseases such as autoimmune encephalomyelitis, graft-versus-host disease, inflammatory bowel disease, and type I diabetes [17][18][19][20][21][22][23].
MSCs secrete a variety of autocrine and paracrine factors including angiogenic factors, chemokines, cytokines, and growth factors that have similar therapeutic effects as systemically administered MSCs do [24]. Previous several studies demonstrated that the intranasal administration of secretome, also known as a conditioned medium, is as secreted molecule from cultured MSCs can convey the same therapeutic actions as the systemic administration of the MSCs themselves [24][25][26]. The MSCs secretome can decrease an allergic airway inflammation by inhibiting Th2 cytokine release and the induction of Treg expansion even without MSCs [24][25][26]. These findings indicate that the main beneficial effects of MSCs are mediated via paracrine actions, although potentially triggered by cell-to-cell contact events.

2. Immunomodulatory Effects of EVs for Allergic Airway Diseases

MSCs could improve the allergic airway disease by inhibiting the proliferation and function of dendritic cells which have an immunomodulatory effect, and which are differentiated into T cells and B cells [27][28][29]. The intravenous injection of MSCs significantly reduced eosinophil infiltration in the nasal mucosa and lung tissue of allergic mouse models and improved the degree of airway hypersensitivity and allergic symptoms [30][31][32]. The MSCs administrated intravenously decreased the number of Th2 cytokines such as IL-4, IL-5, IL-13, and IL-4-positive CD4+ T cells, but they increased the number of Th1 cytokine, IFN- γ and IFN- γ positive CD4+ T cells in the bronchoalveolar lavage (BAL) fluid and lung draining lymph nodes (LLNs) in an AR and asthma mouse model. The MSCs resulted in a significant decrease in the total and ovalbumin (OVA)-specific IgE and IgG1 levels. Tregs, which is characterized by the expression of transcription factor Foxp3, was significantly increased in the LLNs of asthmatic mice after the MSCs administration. Various soluble factors, including TGF-β and PGE2, are secreted by the MSCs that have migrated to the lungs by intravenous or nasal routes of administration, leading to the expansion of Tregs. Anti-inflammatory cytokines (IL-10 and TGF-β) are secreted by Tregs, which ultimately reduce the amount of pulmonary eosinophil infiltration as well as the production of allergy-specific Th2 cytokines and Ig. [30][31][32]. Additionally, in lung histology, eosinophil infiltration and inflammatory cell deposition in the peribronchial and perivascular areas were significantly decreased in the EV group compared to that of the asthma-inducing group [33].
Several studies have reported that the MSC secretomes and MSCs-derived EVs show the same immunomodulatory effects as the stem cells themselves do in allergic airway diseases [24][34][35][36]. Previous studies have shown that bone marrow, umbilical cord, and adipose tissue-derived MSCs and their EVs have the similar immunomodulatory effects in asthmatic mice. Therefore, the efficacy of MSCs-derived EVs does not depend on the MSC source tissue. Furthermore, the systemic and intranasal administration of MSC-derived EVs showed similar immunosuppressive effects in asthmatic mice [34]. De Castro et al. reported that intravenous stem cell culture media and EVs significantly reduced the degree of airway hypersensitivity and eosinophil infiltration of the lung tissues in a mouse model of asthma in the same manner as stem cells did, and the levels of IL-4, IL-5, and IL-6 were significantly reduced. Furthermore, the intravenous administration of human adipose tissue-derived MSCs and EVs reduced the total number of inflammatory cells and the ratio of eosinophils in BAL fluid, IL-5 levels in lung tissues and CD3+ CD4+ T cells in the thymus. However, the number of eosinophils in the lung tissues, the levels of IL-4, IL-13, eotaxin, and CD3+ CD4+ T cells in the BALF, and the pulmonary function showed inconsistent results [35]. Recently, intranasally administrated ASC-derived EVs significantly reduced the degree of allergic airway inflammation and improved AHR through induction of Tregs expansion in asthmatic mice. The intranasal administration of ASC-derived EVs to asthmatic mice resulted in a remarkable reduction of eosinophils and inflammatory cells in the BAL fluid, the serum total and the OVA-specific IgE levels, and the degree of eosinophilic lung inflammation. The level of IL-4 was significantly decreased in the BAL fluid and LLNs, whereas IFN-γ was significantly increased in the BAL fluid. Additionally, CD4+IL-4+ T cells were markedly decreased after an ASC-derived EV treatment, whereas the CD4+CD25+Foxp3+ T cells and CD4+IFN-γ+ T cells were notably increased in the LLNs of asthmatic mice [33].
In an in vitro study, the authors isolated EVs from culture supernatants of murine ASC, which were evaluated the immunomodulatory effects of EVs on Th2-mediated inflammation which was induced by Aspergillus protease antigens in mouse lung epithelial cells and primary lung epithelial cells.
Cho et al. reported that ASC-derived EVs suppressed Th2-mediated inflammation through the upregulation of TGF-β and IL-10 and the downregulation of IL-25 and eotaxin which stimulate the release and recruitment of eosinophils to the sites of inflammation synergistically with IL-5. Furthermore, the ASC-derived EVs induced an anti-inflammatory state in Th2-mediated inflammation through polarization to the M1 and M2 macrophages and dendritic cell maturation for effector T cell induction [36].
The functional enhancement of gene analysis and the microRNA expression pattern analysis, which are methods used to identify a set of overexpressed genes or proteins, have been performed, and studies on the expression pattern and differential expression characteristics of specific genes have been reported.
Kim et al. performed DNA microarray to identify the differentially expressed genes (DEGs) related to the suppression of allergic airway inflammation by ASCs-derived EVs. After the hierarchical clustering of DEGs and after the functional and pathway analysis of the potential DEGs, a total of 249 DEGs were identified, of which 21 were upregulated in the EVs group, resulting in more than 2-fold changes compared to that which was seen in the OVA group. These results suggest that PON1, Bex2, Igfbp6, and Scgb1c1 may be involved in the immunosuppressive mechanism mechanisms of MSCs-derived EVs in allergic airway diseases [37].
Paraoxonase1 (PON1) is a calcium-dependent aryldialkylphosphatase belonging to the paraoxonase (PON) family, and it has antioxidant, anti-adhesive, anti-inflammatory, anti-thrombotic, and anti-apoptotic effects. In addition to asthma, various diseases such as diabetes, rheumatism, arthritis, psoriasis, and systemic lupus erythematosus are also associated with PON1 [38][39][40][41][42][43]. The expression and activity of PON1 in asthmatic patients were significantly lower when they were compared to those of the healthy controls [39][44][45]. Furthermore, PON1 reduced the degree of airway inflammation and airway remodeling and inhibited the lipopolysaccharide (LPS)-induced inflammatory cytokine expression and lung fibroblast proliferation in asthmatic mice, thereby having significant potential effects in allergic airway disease [46]. Bex2 is a protein-coding gene known to be involved in carcinogenesis and it is a regulator of mitochondrial apoptosis and the G1 cell cycle, particularly in breast cancer [47]. Although few reports have been reported on allergic diseases, a recent study reported that Bex2 expression was suppressed by the increased DNA methylation of IL-13 which was induced in allergic airway inflammation [48]. Igfbp6 is a family of insulin-like growth factor (IGF) binding proteins related to the growth inhibitory protein regulating the availability of IGFs. The family of proteins binding to IGFs includes Igfbp1, Igfbp2, Igfbp3, Igfbp4, and Igfbp5 in addition to Igfbp6 [49]. The biological functions of Igfbp can be classified into IGF-independent and IGF-dependent actions. In particular, Igfbp has been reported as a biomarker and a therapeutic target acting on the pathogenesis of various autoimmune diseases, and Igfbp6 was associated with fibroblast proliferation and cell growth in asthmatic patients [50][51]. Fpr1 is a group of G protein-coupled cell surface receptors that have important roles in inflammation and host defenses. Since Fpr1 are expressed across a variety of cell types and interact with structurally diverse chemotactic agents, they either accelerate or inhibit the inflammatory processes upon binding to other ligands [52]. In allergic airway disease, Fpr1 has been reported to stimulate neutrophil chemotaxis and inflammatory cytokine production by phagocytes such as dendritic cells and macrophages [53]. Scgb1c1 is a member of the secretoglobin family of secreted proteins which are found in high concentrations in body fluids of the lungs, lacrimal glands, salivary glands, prostate, uterus, and in other tissues. In the human respiratory mucosa, Scgb1c1 is upregulated by IL-4 and IL-13, and it is downregulated by IFN-γ, and it plays an important role in recognizing and clearance of pathogenic microorganisms in the lung epithelial mucosa [54][55][56]. The important pulmonary genes associated with suppression of allergic airway inflammation by MSC-derived EVs are summarized in Table 1.
Table 1. Pulmonary genes associated with suppression of allergic airway inflammation by MSC-derived EVs.
Although studies on the mechanisms of MSCs-derived EVs on the immunomodulatory effect of ASCs are still lacking, researchers may present a hypothesized schematic based on previous studies. The intranasal administration of EVs isolated from the MSC secretome, including the exosomes and microvesicles, increases the expression of Bex2, PON1, Scgb1c1, and Igfbp6 in the lung tissues of asthmatic mice. These pulmonary genes induce the expansion of Tregs. Tregs secrete regulatory cytokines such as and IL-10 and TGF-β, which reduce pulmonary eosinophil infiltration, allergy-specific Th2 cytokines (IL-4, IL-5, and IL-13), allergy specific IgG1 and IgE production, allergic rhinitis symptoms, and AHR (Figure 1).
Figure 1. Schematic presentation of plausible mechanisms by which MSC-derived EVs regulate the allergic airway diseases. MSC-derived EVs carry microRNAs such as miR-146a-5p, miR-1470, and miR-126-3p and deliver them into lung tissues. Intranasal administration of MSC-derived EVs increases the expression of PON1, Bex2, Igfbp6, and Scgb1c1 in lung tissues of asthmatic mice. These microRNAs and pulmonary genes by MSC-derived EVs induce the expansion of Tregs. Tregs secrete IL-10 and TGF-β, which lead to decrease of allergy-specific Th2 cytokines, lung eosinophil infiltration, and allergy-specific IgG1 and IgE production.


  1. Boulay, M.E.; Boulet, L.-P. The relationships between atopy, rhinitis and asthma: Pathophysiological considerations. Curr. Opin. Allergy Clin. Immunol. 2003, 3, 51–55.
  2. Togias, A. Rhinitis and asthma: Evidence for respiratory system integration. J. Allergy Clin. Immunol. 2003, 111, 1171–1183.
  3. Wilson, M.S.; Taylor, M.D.; Balic, A.; Finney, C.A.; Lamb, J.R.; Maizels, R.M. Suppression of allergic airway inflammation by helminth-induced regulatory T cells. J. Exp. Med. 2005, 202, 1199–1212.
  4. Shi, H.-Z.; Qin, X.-J. CD4CD25 regulatory T lymphocytes in allergy and asthma. Allergy 2005, 60, 986–995.
  5. Biehl, J.K.; Russell, B. Introduction to Stem Cell Therapy. J. Cardiovasc. Nurs. 2009, 24, 98–103.
  6. Law, S.; Chaudhuri, S. Mesenchymal stem cell and regenerative medicine: Regeneration versus immunomodulatory challenges. Am. J. Stem Cells 2013, 2, 22–38.
  7. Tuan, R.S.; Boland, G.; Tuli, R. Adult mesenchymal stem cells and cell-based tissue engineering. Arthritis Res. Ther. 2003, 5, 32–45.
  8. Uccelli, A.; Moretta, L.; Pistoia, V. Mesenchymal stem cells in health and disease. Nat. Rev. Immunol. 2008, 8, 726–736.
  9. Cho, K.-S. Application of Mesenchymal Stem Cells in Rhinologic Fields. Korean J. Otorhinolaryngol.-Head Neck Surg. 2014, 57, 207–213.
  10. Scuteri, A.; Miloso, M.; Foudah, D.; Orcianni, M.; Cavaletti, G.; Trdeici, G. Mesenchymal stem cells neuronal differentiation ability: A real perspective for nervous system repair? Curr. Stem Cell Res. Ther. 2011, 6, 82–92.
  11. Titorencu, I.; Jinga, V.; Constantinescu, E.; Gafencu, A.; Ciohodaru, C.; Manolescu, I.; Zaharia, C.; Simionescu, M. Proliferation, differentiation and characterization of osteoblasts from human BM mesenchymal cells. Cytotherapy 2007, 9, 682–696.
  12. Bhagavati, S.; Xu, W. Isolation and enrichment of skeletal muscle progenitor cells from mouse bone marrow. Biochem. Biophys. Res. Commun. 2004, 318, 119–124.
  13. Liu, T.M.; Martina, M.; Hutmacher, D.W.; Hui, J.H.P.; Lee, E.H.; Lim, B. Identification of Common Pathways Mediating Differentiation of Bone Marrow- and Adipose Tissue-Derived Human Mesenchymal Stem Cells into Three Mesenchymal Lineages. Stem Cells 2007, 25, 750–760.
  14. Delorme, B.; Charbord, P. Culture and Characterization of Human Bone Marrow Mesenchymal Stem Cells. Methods Mol. Med. 2007, 140, 67–81.
  15. Ma, S.; Xie, N.; Li, W.; Yuan, B.; Shi, Y.; Wang, Y. Immunobiology of mesenchymal stem cells. Cell Death Differ. 2014, 21, 216–225.
  16. Shi, M.; Liu, Z.W.; Wang, F.S. Imunomodulatory properties and therapeutic application of mesenchymal stem cells. Clin. Exp. Immunol. 2011, 164, 1–8.
  17. Kim, H.; Shin, T.; Lee, B.; Yu, K.; Seo, Y.; Lee, S.; Seo, M.; Hong, I.; Choi, S.W.; Seo, K.; et al. Human Umbilical Cord Blood Mesenchymal Stem Cells Reduce Colitis in Mice by Activating NOD2 Signaling to COX2. Gastroenterology 2013, 145, 1392–1403.e8.
  18. Németh, K.; Leelahavanichkul, A.; Yuen, P.S.; Mayer, B.; Parmelee, A.; Doi, K.; Robey, P.G.; Leelahavanichkul, K.; Koller, B.H.; Brown, J.M.; et al. Bone marrow stromal cells attenuate sepsis via prostaglandin E2–dependent reprogramming of host macrophages to increase their interleukin-10 production. Nat. Med. 2009, 15, 42–49.
  19. González, M.A.; Gonzalez–Rey, E.; Rico, L.; Büscher, D.; Delgado, M. Adipose-Derived Mesenchymal Stem Cells Alleviate Experimental Colitis by Inhibiting Inflammatory and Autoimmune Responses. Gastroenterology 2009, 136, 978–989.
  20. Augello, A.; Tasso, R.; Negrini, S.M.; Cancedda, R.; Pennesi, G. Cell therapy using allogeneic bone marrow mesenchymal stem cells prevents tissue damage in collagen-induced arthritis. Arthritis Rheum. 2007, 56, 1175–1186.
  21. Lee, R.H.; Seo, M.J.; Reger, R.L.; Spees, J.L.; Pulin, A.A.; Olson, S.D.; Prockop, D.J. Multipotent stromal cells from human marrow home to and promote repair of pancreatic islets and renal glomeruli in diabetic NOD/scid mice. Proc. Natl. Acad. Sci. USA 2006, 103, 17438–17443.
  22. Zappia, E.; Casazza, S.; Pedemonte, E.; Benvenuto, F.; Bonanni, I.; Gerdoni, E.; Giunti, D.; Ceravolo, A.; Cazzanti, F.; Frassoni, F.; et al. Mesenchymal stem cells ameliorate experimental autoimmune encephalomyelitis inducing T-cell anergy. Blood 2005, 106, 1755–1761.
  23. Le Blanc, K.; Rasmusson, I.; Sundberg, B.; Götherström, C.; Hassan, M.; Uzunel, M.; Ringdén, O. Treatment of severe acute graft-versus-host disease with third party haploidentical mesenchymal stem cells. Lancet 2004, 363, 1439–1441.
  24. Yu, H.S.; Park, M.-K.; Kang, S.A.; Cho, K.-S.; Mun, S.J.; Roh, H.-J. Culture supernatant of adipose stem cells can ameliorate allergic airway inflammation via recruitment of CD4+CD25+Foxp3 T cells. Stem Cell Res. Ther. 2017, 8, 1–11.
  25. Ahmadi, M.; Rahbarghazi, R.; Aslani, M.R.; Shahbazfar, A.-A.; Kazemi, M.; Keyhanmanesh, R. Bone marrow mesenchymal stem cells and their conditioned media could potentially ameliorate ovalbumin-induced asthmatic changes. Biomed. Pharmacother. 2017, 85, 28–40.
  26. Ionescu, L.I.; Alphonse, R.S.; Arizmendi, N.; Morgan, B.; Abel, M.; Eaton, F.; Duszyk, M.; Vliagoftis, H.; Aprahamian, T.R.; Walsh, K.; et al. Airway Delivery of Soluble Factors from Plastic-Adherent Bone Marrow Cells Prevents Murine Asthma. Am. J. Respir. Cell Mol. Biol. 2012, 46, 207–216.
  27. Ge, X.; Bai, C.; Yang, J.; Lou, G.; Li, Q.; Chen, R. Effect of mesenchymal stem cells on inhibiting airway remodeling and airway inflammation in chronic asthma. J. Cell. Biochem. 2013, 114, 1595–1605.
  28. Ge, X.; Bai, C.; Yang, J.; Lou, G.; Li, Q.; Chen, R. Intratracheal transplantation of bone marrow-derived mesenchymal stem cells reduced airway inflammation and up-regulated CD4+CD25+regulatory T cells in asthmatic mouse. Cell Biol. Int. 2013, 37, 675–686.
  29. Fu, Q.L.; Chow, Y.Y.; Sun, S.J.; Zeng, Q.X.; Li, H.B.; Shi, J.B.; Sun, Y.-Q.; Wen, W.; Tse, H.F.; Lian, Q.; et al. Mesenchymal stem cells derived from human induced pluripotent stem cells modulate T-cell phenotypes in allergic rhinitis. Allergy 2012, 67, 1215–1222.
  30. Cho, K.-S.; Park, M.-K.; Kang, S.-A.; Park, H.-Y.; Hong, S.-L.; Park, H.-K.; Yu, H.-S.; Roh, H.-J. Adipose-Derived Stem Cells Ameliorate Allergic Airway Inflammation by Inducing Regulatory T Cells in a Mouse Model of Asthma. Mediat. Inflamm. 2014, 2014, 1–12.
  31. Cho, K.-S.; Lee, J.-H.; Park, M.-K.; Park, H.-K.; Yu, H.-S.; Roh, H.-J. Prostaglandin E2 and Transforming Growth Factor-β Play a Critical Role in Suppression of Allergic Airway Inflammation by Adipose-Derived Stem Cells. PLoS ONE 2015, 10, e0131813.
  32. Cho, K.-S.; Park, M.-K.; Mun, S.-J.; Park, H.-Y.; Yu, H.-S.; Roh, H.-J. Indoleamine 2,3-Dioxygenase Is Not a Pivotal Regulator Responsible for Suppressing Allergic Airway Inflammation through Adipose-Derived Stem Cells. PLoS ONE 2016, 11, e0165661.
  33. Mun, S.J.; Kang, S.A.; Park, H.-K.; Yu, H.S.; Cho, K.-S.; Roh, H.-J. Intranasally Administered Extracellular Vesicles from Adipose Stem Cells Have Immunomodulatory Effects in a Mouse Model of Asthma. Stem Cells Int. 2021, 2021, 1–11.
  34. Cruz, F.F.; Borg, Z.D.; Goodwin, M.; Sokocevic, D.; Wagner, D.E.; Coffey, A.; Antunes, M.; Robinson, K.L.; Mitsialis, S.A.; Kourembanas, S.; et al. Systemic Administration of Human Bone Marrow-Derived Mesenchymal Stromal Cell Extracellular Vesicles Ameliorates Aspergillus Hyphal Extract-Induced Allergic Airway Inflammation in Immunocompetent Mice. Stem Cells Transl. Med. 2015, 4, 1302–1316.
  35. de Castro, L.L.; Xisto, D.G.; Kitoko, J.Z.; Cruz, F.F.; Olsen, P.C.; Redondo, P.A.G.; Ferreira, T.P.T.; Weiss, D.J.; Martins, M.A.; Morales, M.M.; et al. Human adipose tissue mesenchymal stromal cells and their extracellular vesicles act differentially on lung mechanics and inflammation in experimental allergic asthma. Stem Cell Res. Ther. 2017, 8, 151.
  36. Cho, K.-S.; Kang, S.A.; Kim, S.-D.; Mun, S.-J.; Yu, H.S.; Roh, H.-J. Dendritic cells and M2 macrophage play an important role in suppression of Th2-mediated inflammation by adipose stem cells-derived extracellular vesicles. Stem Cell Res. 2019, 39, 101500.
  37. Kim, S.-D.; Kang, S.A.; Kim, Y.-W.; Yu, H.S.; Cho, K.-S.; Roh, H.-J. Screening and Functional Pathway Analysis of Pulmonary Genes Associated with Suppression of Allergic Airway Inflammation by Adipose Stem Cell-Derived Extracellular Vesicles. Stem Cells Int. 2020, 27, 5684250.
  38. Bahrehmand, F.; Vaisi-Raygani, A.; Rahimi, Z.; Ahmadi, R.; Kiani, A.; Tavilani, H.; Pourmotabbed, T. Synergistic effects of BuChE non-UU phenotype and paraoxonase (PON1) 55 M allele on the risk of systemic lupus erythematosus: Influence on lipid and lipoprotein metabolism and oxidative stress, preliminary report. Lupus 2014, 23, 263–272.
  39. Sarioglu, N.; Hismiogullari, A.A.; Erel, F.; Demir, D.; Gencer, N. Paraoxonase 1 phenotype and paraoxonase activity in asthmatic patients. Iran. J. Allergy Asthma Immunol. 2015, 14, 60–66.
  40. Tanimoto, N.; Kumon, Y.; Suehiro, T.; Ohkubo, S.; Ikeda, Y.; Nishiya, K.; Hashimoto, K. Serum paraoxonase activity decreases in rheumatoid arthritis. Life Sci. 2003, 72, 2877–2885.
  41. Asefi, M.; Vaisi-Raygani, A.; Bahrehmand, F.; Kiani, A.; Rahimi, Z.; Nomani, H.; Ebrahimi, A.; Tavilani, H.; Pourmotabbed, T. Paraoxonase 1 (PON1) 55 polymorphism, lipid profiles and psoriasis. Br. J. Dermatol. 2012, 167, 1279–1286.
  42. Berg, S.W.V.D.; Jansen, E.H.J.; Kruijshoop, M.; Beekhof, P.K.; Blaak, E.; Van Der Kallen, C.J.; Van Greevenbroek, M.M.; Feskens, E.J.M. Paraoxonase 1 phenotype distribution and activity differs in subjects with newly diagnosed Type 2 diabetes (the CODAM Study). Diabet. Med. 2008, 25, 186–193.
  43. Isik, A.; Koca, S.S.; Ustundag, B.; Celik, H.; Yildirim, A. Paraoxonase and arylesterase levels in rheumatoid arthritis. Clin. Rheumatol. 2007, 26, 342–348.
  44. Tölgyesi, G.; Molnár, V.; Semsei, Á.F.; Kiszel, P.; Ungvári, I.; Pócza, P.; Wiener, Z.; Komlósi, Z.I.; Kunos, L.; Gálffy, G.; et al. Gene expression profiling of experimental asthma reveals a possible role of paraoxonase-1 in the disease. Int. Immunol. 2009, 21, 967–975.
  45. Emin, O.; Hasan, A.; Rusen, D. Plasma paraoxonase, oxidative status level, and their relationship with asthma control test in children with asthma. Allergol. Immunopathol. 2015, 43, 346–352.
  46. Chen, W.; Xie, Z.; Wang, X.; Zhao, J.; Hu, Q.; Chen, Y.; Gao, W.; Liu, Y. Influences of PON1 on airway inflammation and remodeling in bronchial asthma. J. Cell. Biochem. 2018, 119, 793–805.
  47. Naderi, A.; Liu, J.; Bennett, I.C. BEX2 regulates mitochondrial apoptosis and G1 cell cycle in breast cancer. Int. J. Cancer 2010, 126, 1596–1610.
  48. Ooi, A.T.; Ram, S.; Kuo, A.; Gilbert, J.L.; Yan, W.; Pellegrini, M.; Nickerson, D.W.; Chatila, T.; Gomperts, B.N. Identification of an interleukin 13-induced epigenetic signature in allergic airway inflammation. Am. J. Transl. Res. 2012, 4, 219–228.
  49. Ding, H.; Wu, T. Insulin-Like Growth Factor Binding Proteins in Autoimmune Diseases. Front. Endocrinol. 2018, 9, 499.
  50. Vaillancourt, V.T.; Bordeleau, M.; Laviolette, M.; Laprise, C. From expression pattern to genetic association in asthma and asthma-related phenotypes. BMC Res. Notes 2012, 5, 630.
  51. Kostecka, Y.; Blahovec, J. Insulin-like growth factor binding proteins and their biological functions (mini review). Endocr. Regul. 1999, 33, 90–94.
  52. Filina, Y.; Tikhonova, I.; Gabdoulkhakova, A.; Rizvanov, A.; Safronova, V. Mechanisms of ERK phosphorylation triggered via mouse formyl peptide receptor 2. Biochim. Biophys. Acta Mol. Cell Res. 2022, 1869, 119356.
  53. Cardini, S.; Dalli, J.; Fineschi, S.; Perretti, M.; Lungarella, G.; Lucattelli, M. Genetic Ablation of the Fpr1 Gene Confers Protection from Smoking-Induced Lung Emphysema in Mice. Am. J. Respir. Cell Mol. Biol. 2012, 47, 332–339.
  54. Jackson, B.C.; Thompson, D.C.; Wright, M.; McAndrews, M.; Bernard, A.; Nebert, D.W.; Vasiliou, V. Update of the human secretoglobin (SCGB) gene superfamily and an example of ‘evolutionary bloom’ of androgen-binding protein genes within the mouse Scgb gene superfamily. Hum. Genom. 2011, 5, 691–702.
  55. Orysiak, J.; Malczewska-Lenczowska, J.; Bik-Multanowski, M. Expression of SCGB1C1 gene as a potential marker of susceptibility to upper respiratory tract infections in elite athletes—A pilot study. Biol. Sport 2016, 33, 107–110.
  56. Sjödin, A.; Guo, D.; Sørhaug, S.; Bjermer, L.; Henriksson, R.; Hedman, H. Dysregulated secretoglobin expression in human lung cancers. Lung Cancer 2003, 41, 49–56.
Subjects: Immunology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to : ,
View Times: 250
Revisions: 2 times (View History)
Update Date: 08 Dec 2022