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Keeping track of the growing number of biological functions of chitin and its interaction partners in biomedical research.

Koch BE, Stougaard J, Spaink HP - Glycobiology (2015)

Bottom Line: In many studies, these proteins have been found to be involved in immune regulation and in mediating the degradation of chitinous external protective structures of invading pathogens.Finally, we examine the existing literature on zebrafish chitinases, and propose the use of zebrafish as a versatile model to complement the existing murine models.This could especially be of benefit to the exploration of the function of chitinases in infectious diseases using high-throughput approaches and pharmaceutical interventions.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark Leiden University, Institute of Biology, Leiden, The Netherlands.

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Murine in vivo observations of chitin immune-stimulating effects: The experimental approaches have generally been based on delivering chitin particles in liquid suspensions by one of the following routes: (i) intranasal or intratracheal delivery followed by broncheoalveolar lavage (BAL) analysis and histological examinations of lung tissue, (ii) IP injection followed by analysis of peritoneal lavage cell composition or (iii) gastrointestinal delivery by oral gavage followed by histological examination of mucosal barrier integrity and inflammation. In the lung, recent studies established a profound impact of epithelial derived signals, which hitherto have not been studied in other tissues. Repeated delivery with large chitin particles (LCPs) well above phagocytosable size induced IL-25, IL-33 and TSLP, which, via innate ILC2, induced type 2 innate immune responses characterized by tissue eosinophilia and alternative macrophage activation (M2). At the same time, ILC2s exerted an inhibiting effect on type 1 responses which would otherwise be driven by IL-17A released from γδ T cells (Van Dyken et al. 2014). Airway epithelial cells, upon binding of CMP, release CCL2 which further drive M2 (Roy et al. 2012), and CMP was observed to induce the production of IL-10 in BAL macrophages (Da Silva et al. 2009). Single exposure to LCPs leads to an IL-17A driven type 1 immune response which is strongly dependent on TLR-2. It is not known which cells are responsible for perceiving the chitin particles (Da Silva et al. 2008, 2009). In the peritoneum single exposure to CMP leads to phagocytosis-dependent proinflammatory signaling characterized by induction of TNF-α and inducible nitric oxide synthase while downregulating IL-10 expression. LCP induces tissue eosinophilia and M2 characterized by arginase 1 induction by a signaling pathway affected by CHTR2 (Kogiso et al. 2011). The possible signaling influence from the mesothelial cells lining the peritoneal cavity was not investigated. In murine colitis models, CMPs stimulated the accumulation of IL-10 producing cells, presumably alternatively activated macrophages, both at inflamed and non-inflamed sites. They have been shown in vitro to be internalized by dendritic cells which are then thought to stimulate IFN-γ production from CD4+ T cells (CD4+TCs) in the mesenteric lymph nodes (MLN) (Nagatani et al. 2012). Furthermore, CMPs inhibited adherence and invasion of adherent invasive E. coli in IECs (Kawada et al. 2008).
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CWV005F2: Murine in vivo observations of chitin immune-stimulating effects: The experimental approaches have generally been based on delivering chitin particles in liquid suspensions by one of the following routes: (i) intranasal or intratracheal delivery followed by broncheoalveolar lavage (BAL) analysis and histological examinations of lung tissue, (ii) IP injection followed by analysis of peritoneal lavage cell composition or (iii) gastrointestinal delivery by oral gavage followed by histological examination of mucosal barrier integrity and inflammation. In the lung, recent studies established a profound impact of epithelial derived signals, which hitherto have not been studied in other tissues. Repeated delivery with large chitin particles (LCPs) well above phagocytosable size induced IL-25, IL-33 and TSLP, which, via innate ILC2, induced type 2 innate immune responses characterized by tissue eosinophilia and alternative macrophage activation (M2). At the same time, ILC2s exerted an inhibiting effect on type 1 responses which would otherwise be driven by IL-17A released from γδ T cells (Van Dyken et al. 2014). Airway epithelial cells, upon binding of CMP, release CCL2 which further drive M2 (Roy et al. 2012), and CMP was observed to induce the production of IL-10 in BAL macrophages (Da Silva et al. 2009). Single exposure to LCPs leads to an IL-17A driven type 1 immune response which is strongly dependent on TLR-2. It is not known which cells are responsible for perceiving the chitin particles (Da Silva et al. 2008, 2009). In the peritoneum single exposure to CMP leads to phagocytosis-dependent proinflammatory signaling characterized by induction of TNF-α and inducible nitric oxide synthase while downregulating IL-10 expression. LCP induces tissue eosinophilia and M2 characterized by arginase 1 induction by a signaling pathway affected by CHTR2 (Kogiso et al. 2011). The possible signaling influence from the mesothelial cells lining the peritoneal cavity was not investigated. In murine colitis models, CMPs stimulated the accumulation of IL-10 producing cells, presumably alternatively activated macrophages, both at inflamed and non-inflamed sites. They have been shown in vitro to be internalized by dendritic cells which are then thought to stimulate IFN-γ production from CD4+ T cells (CD4+TCs) in the mesenteric lymph nodes (MLN) (Nagatani et al. 2012). Furthermore, CMPs inhibited adherence and invasion of adherent invasive E. coli in IECs (Kawada et al. 2008).

Mentions: When considering the literature as a whole, it is clear that the overall outcome of chitin particle stimulation in terms of inflammatory responses, cellular migration and macrophage activation, is subject to different influences deriving from different cell-types, and observing only one of these factors will lead to confusion and misinterpretations. Figure 2 provides a summary of the observed immune responses to different chitin particles in different tissues.Fig. 2.


Keeping track of the growing number of biological functions of chitin and its interaction partners in biomedical research.

Koch BE, Stougaard J, Spaink HP - Glycobiology (2015)

Murine in vivo observations of chitin immune-stimulating effects: The experimental approaches have generally been based on delivering chitin particles in liquid suspensions by one of the following routes: (i) intranasal or intratracheal delivery followed by broncheoalveolar lavage (BAL) analysis and histological examinations of lung tissue, (ii) IP injection followed by analysis of peritoneal lavage cell composition or (iii) gastrointestinal delivery by oral gavage followed by histological examination of mucosal barrier integrity and inflammation. In the lung, recent studies established a profound impact of epithelial derived signals, which hitherto have not been studied in other tissues. Repeated delivery with large chitin particles (LCPs) well above phagocytosable size induced IL-25, IL-33 and TSLP, which, via innate ILC2, induced type 2 innate immune responses characterized by tissue eosinophilia and alternative macrophage activation (M2). At the same time, ILC2s exerted an inhibiting effect on type 1 responses which would otherwise be driven by IL-17A released from γδ T cells (Van Dyken et al. 2014). Airway epithelial cells, upon binding of CMP, release CCL2 which further drive M2 (Roy et al. 2012), and CMP was observed to induce the production of IL-10 in BAL macrophages (Da Silva et al. 2009). Single exposure to LCPs leads to an IL-17A driven type 1 immune response which is strongly dependent on TLR-2. It is not known which cells are responsible for perceiving the chitin particles (Da Silva et al. 2008, 2009). In the peritoneum single exposure to CMP leads to phagocytosis-dependent proinflammatory signaling characterized by induction of TNF-α and inducible nitric oxide synthase while downregulating IL-10 expression. LCP induces tissue eosinophilia and M2 characterized by arginase 1 induction by a signaling pathway affected by CHTR2 (Kogiso et al. 2011). The possible signaling influence from the mesothelial cells lining the peritoneal cavity was not investigated. In murine colitis models, CMPs stimulated the accumulation of IL-10 producing cells, presumably alternatively activated macrophages, both at inflamed and non-inflamed sites. They have been shown in vitro to be internalized by dendritic cells which are then thought to stimulate IFN-γ production from CD4+ T cells (CD4+TCs) in the mesenteric lymph nodes (MLN) (Nagatani et al. 2012). Furthermore, CMPs inhibited adherence and invasion of adherent invasive E. coli in IECs (Kawada et al. 2008).
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4373397&req=5

CWV005F2: Murine in vivo observations of chitin immune-stimulating effects: The experimental approaches have generally been based on delivering chitin particles in liquid suspensions by one of the following routes: (i) intranasal or intratracheal delivery followed by broncheoalveolar lavage (BAL) analysis and histological examinations of lung tissue, (ii) IP injection followed by analysis of peritoneal lavage cell composition or (iii) gastrointestinal delivery by oral gavage followed by histological examination of mucosal barrier integrity and inflammation. In the lung, recent studies established a profound impact of epithelial derived signals, which hitherto have not been studied in other tissues. Repeated delivery with large chitin particles (LCPs) well above phagocytosable size induced IL-25, IL-33 and TSLP, which, via innate ILC2, induced type 2 innate immune responses characterized by tissue eosinophilia and alternative macrophage activation (M2). At the same time, ILC2s exerted an inhibiting effect on type 1 responses which would otherwise be driven by IL-17A released from γδ T cells (Van Dyken et al. 2014). Airway epithelial cells, upon binding of CMP, release CCL2 which further drive M2 (Roy et al. 2012), and CMP was observed to induce the production of IL-10 in BAL macrophages (Da Silva et al. 2009). Single exposure to LCPs leads to an IL-17A driven type 1 immune response which is strongly dependent on TLR-2. It is not known which cells are responsible for perceiving the chitin particles (Da Silva et al. 2008, 2009). In the peritoneum single exposure to CMP leads to phagocytosis-dependent proinflammatory signaling characterized by induction of TNF-α and inducible nitric oxide synthase while downregulating IL-10 expression. LCP induces tissue eosinophilia and M2 characterized by arginase 1 induction by a signaling pathway affected by CHTR2 (Kogiso et al. 2011). The possible signaling influence from the mesothelial cells lining the peritoneal cavity was not investigated. In murine colitis models, CMPs stimulated the accumulation of IL-10 producing cells, presumably alternatively activated macrophages, both at inflamed and non-inflamed sites. They have been shown in vitro to be internalized by dendritic cells which are then thought to stimulate IFN-γ production from CD4+ T cells (CD4+TCs) in the mesenteric lymph nodes (MLN) (Nagatani et al. 2012). Furthermore, CMPs inhibited adherence and invasion of adherent invasive E. coli in IECs (Kawada et al. 2008).
Mentions: When considering the literature as a whole, it is clear that the overall outcome of chitin particle stimulation in terms of inflammatory responses, cellular migration and macrophage activation, is subject to different influences deriving from different cell-types, and observing only one of these factors will lead to confusion and misinterpretations. Figure 2 provides a summary of the observed immune responses to different chitin particles in different tissues.Fig. 2.

Bottom Line: In many studies, these proteins have been found to be involved in immune regulation and in mediating the degradation of chitinous external protective structures of invading pathogens.Finally, we examine the existing literature on zebrafish chitinases, and propose the use of zebrafish as a versatile model to complement the existing murine models.This could especially be of benefit to the exploration of the function of chitinases in infectious diseases using high-throughput approaches and pharmaceutical interventions.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Biology and Genetics, Aarhus University, Aarhus C, Denmark Leiden University, Institute of Biology, Leiden, The Netherlands.

Show MeSH
Related in: MedlinePlus