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1

Brown, T. A. "Immunity at Mucosal Surfaces." Advances in Dental Research 10, no. 1 (April 1996): 62–65. http://dx.doi.org/10.1177/08959374960100011201.

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The mucosae form a barrier between our bodies and a hostile external environment. Diseases and extrinsic factors which impair mucosal function may lead to serious consequences. The mucosal immune system is the primary mediator of specific immunity at mucosal surfaces. As such, it is responsible for maintaining homeostasis and for defense against both overt and opportunistic pathogens. For this reason, it is also the target of many new vaccine strategies for the induction of mucosal immunity. This brief review will examine the mucosal immune system, its role in maintaining the integrity of the mucosa, and some of the strategies aimed at enhancing specific immunity.
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2

Dougan, Gordon, Marjan Ghaem–Maghami, Derek Pickard, Gad Frankel, Gill Douce, Simon Clare, Sarah Dunstan, and Cameron Simmons. "The immune responses to bacterial antigens encountered in vivo at mucosal surfaces." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1397 (May 28, 2000): 705–12. http://dx.doi.org/10.1098/rstb.2000.0610.

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Mammals have evolved a sophisticated immune system for handling antigens encountered at their mucosal surfaces. The way in which mucosally delivered antigens are handled influences our ability to design effective mucosal vaccines. Live attenuated derivatives of pathogens are one route towards the development of mucosal vaccines. However, some molecules, described as mucosal immunogens, are inherently immunogenic at mucosal surfaces. Studies on mucosal immunogens may facilitate the identification of common characteristics that contribute to mucosal immunogenicity and aid the development of novel, non–living mucosal vaccines and immunostimulators.
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3

Oldham, Geoffrey. "Aspects of Immunology of the Gut and Rotavirus Infection." Proceedings of the British Society of Animal Production (1972) 1993 (March 1993): 32. http://dx.doi.org/10.1017/s0308229600023618.

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The major portal of entry for most pathogenic microorganisms is the mucosal surface. It seems reasonable therefore that the host in its turn should possess substantial immune defences at the mucosae to provide protection against these insults. Enteric infections usually result in at least some degree of specific protection against a subsequent infection with the same organism. However artificial induction of mucosal immunity has proved difficult. Clearly, as yet, we do not have a full understanding of the inductive events involved in the generation of mucosal immune responses or the immune mechanisms operating at mucosal surfaces. In this paper I will attempt to briefly review the main aspects of mucosal immunity concentrating on the gut as the model mucosal surface.
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4

Feng, Fengling, Ziyu Wen, Jiaoshan Chen, Yue Yuan, Congcong Wang, and Caijun Sun. "Strategies to Develop a Mucosa-Targeting Vaccine against Emerging Infectious Diseases." Viruses 14, no. 3 (March 3, 2022): 520. http://dx.doi.org/10.3390/v14030520.

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Numerous pathogenic microbes, including viruses, bacteria, and fungi, usually infect the host through the mucosal surfaces of the respiratory tract, gastrointestinal tract, and reproductive tract. The mucosa is well known to provide the first line of host defense against pathogen entry by physical, chemical, biological, and immunological barriers, and therefore, mucosa-targeting vaccination is emerging as a promising strategy for conferring superior protection. However, there are still many challenges to be solved to develop an effective mucosal vaccine, such as poor adhesion to the mucosal surface, insufficient uptake to break through the mucus, and the difficulty in avoiding strong degradation through the gastrointestinal tract. Recently, increasing efforts to overcome these issues have been made, and we herein summarize the latest findings on these strategies to develop mucosa-targeting vaccines, including a novel needle-free mucosa-targeting route, the development of mucosa-targeting vectors, the administration of mucosal adjuvants, encapsulating vaccines into nanoparticle formulations, and antigen design to conjugate with mucosa-targeting ligands. Our work will highlight the importance of further developing mucosal vaccine technology to combat the frequent outbreaks of infectious diseases.
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5

Parrott, D. M. V. "Mucosal immunity and infections at mucosal surfaces." Immunology Today 10, no. 4 (April 1989): 138. http://dx.doi.org/10.1016/0167-5699(89)90248-x.

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6

Gryboski, Joyce D. "Mucosal immunity and infections at mucosal surfaces." Gastroenterology 96, no. 3 (March 1989): 952–53. http://dx.doi.org/10.1016/0016-5085(89)90935-9.

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7

Russell, Michael W., and Pearay L. Ogra. "Mucosal Decisions: Tolerance and Responsiveness at Mucosal Surfaces." Immunological Investigations 39, no. 4-5 (January 1, 2010): 297–302. http://dx.doi.org/10.3109/08820131003729927.

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8

Smith, Phillip D., and Ruizhong Shen. "Target Cells for HIV-1/SIV Infection in Mucosal Tissue." Current Immunology Reviews 15, no. 1 (April 12, 2019): 28–35. http://dx.doi.org/10.2174/1573395514666180531072126.

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The mucosal surfaces of the genital and gastrointestinal tracts are the routes by which HIV-1 is acquired, excluding persons infected parenterally. Identification of the mucosal target cells and the receptors by which HIV-1 enters these cells is fundamental to elucidating the biology of HIV-1 transmission. The mucosal target cells include epithelial cells, dendritic cells, Langerhans cells, CD4+ T-cells, macrophages and even mast cells, but the contribution of each cell type is highly dependent on the mucosal surface - genital versus gastrointestinal. Importantly, mucosal target cells may also play key roles in the immunobiology and latency of HIV-1 infection. Given the pivotal role of mucosal cells in HIV-1 transmission and pathogenesis, an effective vaccine to bring the HIV-1 pandemic under control must be effective at the level of the key target cells in both the genital and gastrointestinal mucosae.
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9

Okamura, Hiroshi, Eiji Yumoto, and Kazunori Okamoto. "Wound Healing of Canine Vocal Folds after Phonosurgery." Annals of Otology, Rhinology & Laryngology 96, no. 4 (July 1987): 425–28. http://dx.doi.org/10.1177/000348948709600415.

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To develop phonosurgical techniques, the authors investigated the healing mechanisms of wounds on the vocal folds of canine larynges, and devised a method to cover the raw surfaces of such wounds. To restore the normal physiologic properties of the vocal folds, the normal mucosa should be removed as little as possible in phonosurgery. When the mucosa of the vocal folds is extensively removed by surgical intervention and the raw surface cannot be covered with the local pedicle flap, it should be covered with a free mucosal flap. We found an activated human fibrinogen concentrate, which is a biologic tissue adhesive, to be suitable for adhering a free mucosal flap to the raw surface by a laryngomicrosurgical approach.
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10

Diaz, Patricia I., Zhihong Xie, Takanori Sobue, Angela Thompson, Basak Biyikoglu, Austin Ricker, Laertis Ikonomou, and Anna Dongari-Bagtzoglou. "Synergistic Interaction between Candida albicans and Commensal Oral Streptococci in a NovelIn VitroMucosal Model." Infection and Immunity 80, no. 2 (November 21, 2011): 620–32. http://dx.doi.org/10.1128/iai.05896-11.

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ABSTRACTCandida albicansis a commensal colonizer of the gastrointestinal tract of humans, where it coexists with highly diverse bacterial communities. It is not clear whether this interaction limits or promotes the potential ofC. albicansto become an opportunistic pathogen. Here we investigate the interaction betweenC. albicansand three species of streptococci from the viridans group, which are ubiquitous and abundant oral commensal bacteria. The ability ofC. albicansto form biofilms withStreptococcus oralis,Streptococcus sanguinis, orStreptococcus gordoniiwas investigated using flow cell devices that allow abiotic biofilm formation under salivary flow. In addition, we designed a novel flow cell system that allows mucosal biofilm formation under conditions that mimic the environment in the oral and esophageal mucosae. It was observed thatC. albicansand streptococci formed a synergistic partnership whereC. albicanspromoted the ability of streptococci to form biofilms on abiotic surfaces or on the surface of an oral mucosa analogue. The increased ability of streptococci to form biofilms in the presence ofC. albicanscould not be explained by a growth-stimulatory effect since the streptococci were unaffected in their growth in planktonic coculture withC. albicans. Conversely, the presence of streptococci increased the ability ofC. albicansto invade organotypic models of the oral and esophageal mucosae under conditions of salivary flow. Moreover, characterization of mucosal invasion by the biofilm microorganisms suggested that the esophageal mucosa is more permissive to invasion than the oral mucosa. In summary,C. albicansand commensal oral streptococci display a synergistic interaction with implications for the pathogenic potential ofC. albicansin the upper gastrointestinal tract.
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11

Foss, Dennis L., and Michael P. Murtaugh. "Mechanisms of vaccine adjuvanticity at mucosal surfaces." Animal Health Research Reviews 1, no. 1 (June 2000): 3–24. http://dx.doi.org/10.1017/s1466252300000025.

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AbstractThe vast majority of pathogens invade via mucosal surfaces, including those of the intestine. Vaccination directly on these surfaces may induce local protective immunity and prevent infection and disease. Although vaccine delivery to the gut mucosa is fraught with obstacles, immunization can be enhanced using adjuvants with properties specific to intestinal immunity. In this review, we present three general mechanisms of vaccine adjuvant function as originally described by Freund, and we discuss these principles with respect to intestinal adjuvants in general and to the prototypical mucosal adjuvant, cholera toxin. The key property of intestinal adjuvants is to induce an immunogenic context for the presentation of the vaccine antigen. The success of oral vaccine adjuvants is determined by their ability to induce a controlled inflammatory response in the gut-associated lymphoid tissues, characterized by the expression of various costimulatory molecules and cytokines. An understanding of the specific molecular mechanisms of adjuvanticity in the gut will allow the rational development of safe and effective oral vaccines.
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12

Meeusen, Els N. "Exploiting mucosal surfaces for the development of mucosal vaccines." Vaccine 29, no. 47 (November 2011): 8506–11. http://dx.doi.org/10.1016/j.vaccine.2011.09.010.

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13

Smith, Aileen Robertson, Sandra Macfarlane, Elizabeth Furrie, Shakil Ahmed, Bahram Bahrami, Nigel Reynolds, and George Tennant Macfarlane. "Microbiological and immunological effects of enteral feeding on the upper gastrointestinal tract." Journal of Medical Microbiology 60, no. 3 (March 1, 2011): 359–65. http://dx.doi.org/10.1099/jmm.0.026401-0.

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Enteral feeding via a percutaneous endoscopic gastrostomy tube is required for nutritional support in patients with dysphagia. Enteral tube feeding bypasses the innate defence mechanisms in the upper gastrointestinal tract. This study examined the surface-associated microbial populations and immune response in the gastric and duodenal mucosae of eight enteral nutrition (EN) patients and ten controls. Real-time PCR and fluorescence in situ hybridization were employed to assess microbiota composition and mucosal pro-inflammatory cytokine expression. The results showed that EN patients had significantly higher levels of bacterial DNA in mucosal biopsies from the stomach and duodenum (P<0.05) than the controls, and that enterobacteria were the predominant colonizing species on mucosal surfaces in these individuals. Expression of the pro-inflammatory cytokines interleukin (IL)-1α, IL-6 and tumour necrosis factor-α was significantly higher in gastric and small intestinal mucosae from patients fed normal diets in comparison with those receiving EN (P<0.05). These results indicate that EN can lead to significant bacterial overgrowth on upper gastrointestinal tract mucosae and a significantly diminished pro-inflammatory cytokine response.
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14

McGhee, Jerry R., and Jiri Mestecky. "In Defense of Mucosal Surfaces." Infectious Disease Clinics of North America 4, no. 2 (June 1990): 315–41. http://dx.doi.org/10.1016/s0891-5520(20)30344-5.

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15

Gary, Ebony N., and Michele A. Kutzler. "Defensive Driving: Directing HIV-1 Vaccine-Induced Humoral Immunity to the Mucosa with Chemokine Adjuvants." Journal of Immunology Research 2018 (December 13, 2018): 1–14. http://dx.doi.org/10.1155/2018/3734207.

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A myriad of pathogens gain access to the host via the mucosal route; thus, vaccinations that protect against mucosal pathogens are critical. Pathogens such as HIV, HSV, and influenza enter the host at mucosal sites such as the intestinal, urogenital, and respiratory tracts. All currently licensed vaccines mediate protection by inducing the production of antibodies which can limit pathogen replication at the site of infection. Unfortunately, parenteral vaccination rarely induces the production of an antigen-specific antibody at mucosal surfaces and thus relies on transudation of systemically generated antibody to mucosal surfaces to mediate protection. Mucosa-associated lymphoid tissues (MALTs) consist of a complex network of immune organs and tissues that orchestrate the interaction between the host, commensal microbes, and pathogens at these surfaces. This complexity necessitates strict control of the entry and exit of lymphocytes in the MALT. This control is mediated by chemoattractant chemokines or cytokines which recruit immune cells expressing the cognate receptors and adhesion molecules. Exploiting mucosal chemokine trafficking pathways to mobilize specific subsets of lymphocytes to mucosal tissues in the context of vaccination has improved immunogenicity and efficacy in preclinical models. This review describes the novel use of MALT chemokines as vaccine adjuvants. Specific attention will be placed upon the use of such adjuvants to enhance HIV-specific mucosal humoral immunity in the context of prophylactic vaccination.
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16

Bhat, Mohd Y., Ashok Channa, Bilal A. Paray, Mohammed K. Al-Sadoon, and Irfan A. Rather. "Morphological study of the gastrointestinal tract of the snow trout, Schizothorax esocinus (Actinopterygii: Cypriniformes)." Zoologia 36 (November 13, 2019): 1–7. http://dx.doi.org/10.3897/zoologia.36.e31791.

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The present study aimed to investigate the macroscopic structure of the gastrointestinal tract (GIT) of Schizothorax esocinus Heckel, 1838. The surface architecture of the buccopharynx, oesophagus and the entire intestinal tract of S. esocinus has been examined under scanning electron microscope (SEM) after fixing in 2.5% glutaraldehyde buffered with 0.1 M sodium cacodylate at pH 7.3 for 18–48 hours and post-fixation for two hours at room temperature in 1% osmium tetra oxide buffered at pH 7.3 with 0.1 M cacodylate. The mucosal surface of buccopharynx, esophagus, intestinal bulb, and intestine reveal prominent longitudinal major or primary mucosal folds which are further subdivided into the series of irregular and well-circumscribed folds called minor or secondary folds. However, in the intestinal bulb and intestine, the longitudinal major or primary folds themselves form wavy or zigzagging patterns along the mucosal surface. The fine structure of the surface epithelium further shows that the apical surfaces of the epithelial cells are ped with finger-print like microridges, arranged in various patterns and regularly spaced. The rectal mucosa, on the other hand, displays a highly irregular type of major mucosal folds. The separation can’t be seen between major mucosal folds. A thin film of mucous spread over the mucosal folds and the numerous pores through which mucous cells release their content has also been noted along the rectal mucosa. This investigation suggests the possible role of different digestive organs in relation to feeding, digestion, storage, absorption, and various other physiological processes, thereby providing a knowledge necessary to the understanding of pathological or physiological alterations in both aquaculture and natural environment.
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17

Fujimoto, Kosuke, and Satoshi Uematsu. "Development of prime–boost-type next-generation mucosal vaccines." International Immunology 32, no. 9 (December 28, 2019): 597–603. http://dx.doi.org/10.1093/intimm/dxz085.

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Abstract Our bodies are constantly exposed to a wide variety of pathogenic micro-organisms through mucosal sites. Therefore, effective vaccines that can protect at the mucosa are vital; however, only a few clinically established mucosal vaccines are available. Although conventional injectable vaccines can induce antigen-specific serum immunoglobulin G (IgG) and prevent severe infection, it is difficult to efficiently inhibit the invasion of pathogens at mucosal surfaces because of the inadequate ability to induce antigen-specific IgA. Recently, we have developed a parenteral vaccine with emulsified curdlan and CpG oligodeoxynucleotides and reported its application. Unlike other conventional injectable vaccines, this immunization contributes to the induction of antigen-specific mucosal and systemic immune responses. Even if antigen-specific IgA at the mucosa disappears, this immunization can induce high-titer IgA after boosting with a small amount of antigen on the target mucosal surface. Indeed, vaccination with Streptococcus pneumoniae antigen effectively prevented lung infection induced by this bacterium. In addition, vaccination with Clostridium ramosum, which is a representative pathobiont associated with obesity and diabetes in humans, reduced obesity in mice colonized with this microorganism. This immunization approach might be an effective treatment for intestinal bacteria-mediated diseases that have been difficult to regulate so far, as well as common infectious diseases.
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18

Harrell, Jaikin, Lisa A. Morici, and James B. McLachlan. "The use of outer membrane vesicles as novel, mucosal adjuvants against intracellular bactiera." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 181.09. http://dx.doi.org/10.4049/jimmunol.208.supp.181.09.

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Abstract Many pathogens first enter the body via mucosal surfaces where they can then invade and disseminate systemically to cause disease. Despite this, most vaccines are given parenterally and are unable to induce mucosal immunity. Immunizing directly at the mucosa could solve this problem, however delivering vaccines at these surfaces often doesn’t invoke robust immunity. One way to alleviate this is to use adjuvants that can evoke an immune response. Most adjuvants, like aluminum salts, are unable to induce mucosal immunity and so novel adjuvants must be employed. Outer membrane vesicles (OMVs) from Burkholderia pseudomallei are potent immune mediators and have been shown to have adjuvant capabilities. The goal of this study is to highlight the role of OMVs as a novel adjuvant that can be used in the next generation of mucosal vaccines. To test this, we created an OMV-adjuvanted inactivated whole-cell vaccine against two intracellular pathogens – Salmonella Typhimurium and Francisella holarctica LVS that could be delivered mucosally. An oral vaccine against S. Typhimurium adjuvanted with OMVs showed protection against lethal challenge in addition to evoking antigen specific CD4 T cells, B cells, and anti-Salmonella antibodies. These antibodies induced greater bacterial killing in macrophages. We are currently exploring an OMV-adjuvanted oropharyngeally delivered vaccine against F. holarctica LVS. Immunity against Francisella requires both CD4 and CD8 T cells and we are determining how an OMV-adjuvanted vaccine will influence these immune cell populations. This study represents a novel approach to mucosal vaccines using OMVs as adjuvants. Supported by NIH U01 AI124289 NIH BAA HHSN72201800045C
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19

Tang, Jie, Larry Cai, Chuanfei Xu, Si Sun, Yuheng Liu, Joseph Rosenecker, and Shan Guan. "Nanotechnologies in Delivery of DNA and mRNA Vaccines to the Nasal and Pulmonary Mucosa." Nanomaterials 12, no. 2 (January 11, 2022): 226. http://dx.doi.org/10.3390/nano12020226.

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Recent advancements in the field of in vitro transcribed mRNA (IVT-mRNA) vaccination have attracted considerable attention to such vaccination as a cutting-edge technique against infectious diseases including COVID-19 caused by SARS-CoV-2. While numerous pathogens infect the host through the respiratory mucosa, conventional parenterally administered vaccines are unable to induce protective immunity at mucosal surfaces. Mucosal immunization enables the induction of both mucosal and systemic immunity, efficiently removing pathogens from the mucosa before an infection occurs. Although respiratory mucosal vaccination is highly appealing, successful nasal or pulmonary delivery of nucleic acid-based vaccines is challenging because of several physical and biological barriers at the airway mucosal site, such as a variety of protective enzymes and mucociliary clearance, which remove exogenously inhaled substances. Hence, advanced nanotechnologies enabling delivery of DNA and IVT-mRNA to the nasal and pulmonary mucosa are urgently needed. Ideal nanocarriers for nucleic acid vaccines should be able to efficiently load and protect genetic payloads, overcome physical and biological barriers at the airway mucosal site, facilitate transfection in targeted epithelial or antigen-presenting cells, and incorporate adjuvants. In this review, we discuss recent developments in nucleic acid delivery systems that target airway mucosa for vaccination purposes.
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20

Allen, Adrian, and Gunnar Flemström. "Gastroduodenal mucus bicarbonate barrier: protection against acid and pepsin." American Journal of Physiology-Cell Physiology 288, no. 1 (January 2005): C1—C19. http://dx.doi.org/10.1152/ajpcell.00102.2004.

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Secretion of bicarbonate into the adherent layer of mucus gel creates a pH gradient with a near-neutral pH at the epithelial surfaces in stomach and duodenum, providing the first line of mucosal protection against luminal acid. The continuous adherent mucus layer is also a barrier to luminal pepsin, thereby protecting the underlying mucosa from proteolytic digestion. In this article we review the present state of the gastroduodenal mucus bicarbonate barrier two decades after the first supporting experimental evidence appeared. The primary function of the adherent mucus gel layer is a structural one to create a stable, unstirred layer to support surface neutralization of acid and act as a protective physical barrier against luminal pepsin. Therefore, the emphasis on mucus in this review is on the form and role of the adherent mucus gel layer. The primary function of the mucosal bicarbonate secretion is to neutralize acid diffusing into the mucus gel layer and to be quantitatively sufficient to maintain a near-neutral pH at the mucus-mucosal surface interface. The emphasis on mucosal bicarbonate in this review is on the mechanisms and control of its secretion and the establishment of a surface pH gradient. Evidence suggests that under normal physiological conditions, the mucus bicarbonate barrier is sufficient for protection of the gastric mucosa against acid and pepsin and is even more so for the duodenum.
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21

Cabillon, Nikko, and Carlo Lazado. "Mucosal Barrier Functions of Fish under Changing Environmental Conditions." Fishes 4, no. 1 (January 10, 2019): 2. http://dx.doi.org/10.3390/fishes4010002.

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The skin, gills, and gut are the most extensively studied mucosal organs in fish. These mucosal structures provide the intimate interface between the internal and external milieus and serve as the indispensable first line of defense. They have highly diverse physiological functions. Their role in defense can be highlighted in three shared similarities: their microanatomical structures that serve as the physical barrier and hold the immune cells and the effector molecules; the mucus layer, also a physical barrier, contains an array of potent bioactive molecules; and the resident microbiota. Mucosal surfaces are responsive and plastic to the different changes in the aquatic environment. The direct interaction of the mucosa with the environment offers some important information on both the physiological status of the host and the conditions of the aquatic environment. Increasing attention has been directed to these features in the last year, particularly on how to improve the overall health of the fish through manipulation of mucosal functions and on how the changes in the mucosa, in response to varying environmental factors, can be harnessed to improve husbandry. In this short review, we highlight the current knowledge on how mucosal surfaces respond to various environmental factors relevant to aquaculture and how they may be exploited in fostering sustainable fish farming practices, especially in controlled aquaculture environments.
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22

Nikou, Spyridoula-Angeliki, Nessim Kichik, Rhys Brown, Nicole Ponde, Jemima Ho, Julian Naglik, and Jonathan Richardson. "Candida albicans Interactions with Mucosal Surfaces during Health and Disease." Pathogens 8, no. 2 (April 22, 2019): 53. http://dx.doi.org/10.3390/pathogens8020053.

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Flexible adaptation to the host environment is a critical trait that underpins the success of numerous microbes. The polymorphic fungus Candida albicans has evolved to persist in the numerous challenging niches of the human body. The interaction of C. albicans with a mucosal surface is an essential prerequisite for fungal colonisation and epitomises the complex interface between microbe and host. C. albicans exhibits numerous adaptations to a healthy host that permit commensal colonisation of mucosal surfaces without provoking an overt immune response that may lead to clearance. Conversely, fungal adaptation to impaired immune fitness at mucosal surfaces enables pathogenic infiltration into underlying tissues, often with devastating consequences. This review will summarise our current understanding of the complex interactions that occur between C. albicans and the mucosal surfaces of the human body.
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23

MCGEE, Z. A., R. H. LATHAM, and E. N. ROBINSON. "Molecular mechanisms of interaction of mucosal pathogens with human mucosal surfaces." Pediatric Infectious Disease Journal 5, Supplement (January 1986): 83–87. http://dx.doi.org/10.1097/00006454-198601001-00014.

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24

Wootton, Lucie. "A new barrier at mucosal surfaces." Nature Reviews Microbiology 11, no. 7 (June 14, 2013): 431. http://dx.doi.org/10.1038/nrmicro3064.

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25

King, Brent R. "Mucosal Surfaces for Noninvasive Drug Administration." Emergency Medicine News 27, no. 12 (December 2005): 34. http://dx.doi.org/10.1097/00132981-200512000-00022.

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26

Senior, Kathryn. "Molecular shield that protects mucosal surfaces." Lancet 359, no. 9310 (March 2002): 950. http://dx.doi.org/10.1016/s0140-6736(02)08049-2.

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27

Sansonetti, Philippe J. "War and peace at mucosal surfaces." Nature Reviews Immunology 4, no. 12 (December 2004): 953–64. http://dx.doi.org/10.1038/nri1499.

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28

Miller, H. R. P. "Gastrointestinal mucus, a medium for survival and for elimination of parasitic nematodes and protozoa." Parasitology 94, S1 (January 1987): S77—S100. http://dx.doi.org/10.1017/s0031182000085838.

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Mucus is a sticky visco-elastic material which coats all mucosal surfaces. Florey, in 1955, noted the following three functions for gastrointestinal mucus: protection of the underlying mucosa from chemical and physical injury, lubrication of the mucosal surface to facilitate passage of luminal contents, and removal of parasites by binding and entrapment. In the 31 years since Florey's review, detailed analyses of the composition of mucus and of the biochemistry of mucin glycoproteins, as well as measurements of the physical properties of mucus from different organs and sites have yielded information at the molecular level which provide additional support for his views on its function (Allen, 1981; Forstner, Wesley & Forstner, 1982).
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29

Gómez-Duarte, Oscar G., and Pearay L. Ogra. "Development of Mucosal Immunity: Functional Interactions with Mucosal Microbiome in Health and Disease." Current Immunology Reviews 15, no. 2 (December 18, 2019): 154–65. http://dx.doi.org/10.2174/1573395515666190225153529.

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The mucosal surfaces and the skin are the primary sites of interactions between the mammalian host and the external environment. These sites are exposed continuously to the diverse components of the environment, including subcellular, unicellular and multicellular organisms, dietary agents and food products; and numerous other soluble or cellular air or water borne products. The development of innate and adaptive immunity in the mucosal surfaces and the skin are the principal mechanism of mammalian defense evolved to date, in order to maintain effective homeostatic balance between the host and the external environment. The innate immune functions are mediated by a number of host specific Pathogen Recognition Receptors (PRR), designed to recognize unique Pathogen Associated Molecular Patterns (PAMP), essential to the molecular structure of the microorganism. The major components of specific adaptive immunity in the mucosal surfaces include the organized antigen-reactive lymphoid follicles in different inductive mucosal sites and the effector sites of the lamina propria and sub-epithelial regions, which contain lymphoid and plasma cells, derived by the homing of antigen sensitized cells from the inductive sites. The acquisition of environmental microbiome by the neonate in its mucosal surfaces and the skin, which begins before or immediately after birth, has been shown to play a critical and complex role in the development of mucosal immunity. This report provides an overview of the mammalian microbiome and highlights its role in the evolution and functional development of immunologic defenses in the mucosal surface under normal physiologic conditions and during infectious and non-infectious inflammatory pathologic states associated with altered microbiota.
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Kozlowski, Pamela A., and Anna Aldovini. "Mucosal Vaccine Approaches for Prevention of HIV and SIV Transmission." Current Immunology Reviews 15, no. 1 (April 12, 2019): 102–22. http://dx.doi.org/10.2174/1573395514666180605092054.

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Optimal protective immunity to HIV will likely require that plasma cells, memory B cells and memory T cells be stationed in mucosal tissues at portals of viral entry. Mucosal vaccine administration is more effective than parenteral vaccine delivery for this purpose. The challenge has been to achieve efficient vaccine uptake at mucosal surfaces, and to identify safe and effective adjuvants, especially for mucosally administered HIV envelope protein immunogens. Here, we discuss strategies used to deliver potential HIV vaccine candidates in the intestine, respiratory tract, and male and female genital tract of humans and nonhuman primates. We also review mucosal adjuvants, including Toll-like receptor agonists, which may adjuvant both mucosal humoral and cellular immune responses to HIV protein immunogens.
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31

Seong, Seung-Yong, Nam-Hyuk Cho, Ick Chan Kwon, and Seo Young Jeong. "Protective Immunity of Microsphere-Based Mucosal Vaccines against Lethal Intranasal Challenge withStreptococcus pneumoniae." Infection and Immunity 67, no. 7 (July 1, 1999): 3587–92. http://dx.doi.org/10.1128/iai.67.7.3587-3592.1999.

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ABSTRACT Mucosal vaccination of capsular polysaccharide (PS) ofStreptococcus pneumoniae and subsequent creation of the first line of immunological defense in mucosa were examined. Mucosal as well as systemic antibody responses to PS were evoked by peroral or intranasal immunization of BALB/c mice with PS-cholera toxin B subunit (CTB) conjugates entrapped in the alginate microspheres (AM). The bacterial colonization at the lung mucosa was most profoundly inhibited (<95%) by intranasal immunization with the naked conjugate (PS-CTB). The mice vaccinated orally with encapsulated conjugate [AM(PS-CTB)] showed significant reduction on the level of pneumococcal bacteremia (<99%). Eighty percent of the mice perorally immunized with AM (PS-CTB) were protected from lethal intranasal challenge with S. pneumoniae, whereas more than 60% of the mice in the other control groups died of infection. Our novel approach may prove to be important in the development of a mucosal vaccine that will provide protection of mucosal surfaces of host.
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Legrand, Thibault P. R. A., James W. Wynne, Laura S. Weyrich, and Andrew P. A. Oxley. "Investigating Both Mucosal Immunity and Microbiota in Response to Gut Enteritis in Yellowtail Kingfish." Microorganisms 8, no. 9 (August 20, 2020): 1267. http://dx.doi.org/10.3390/microorganisms8091267.

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The mucosal surfaces of fish play numerous roles including, but not limited to, protection against pathogens, nutrient digestion and absorption, excretion of nitrogenous wastes and osmotic regulation. During infection or disease, these surfaces act as the first line of defense, where the mucosal immune system interacts closely with the associated microbiota to maintain homeostasis. This study evaluated microbial changes across the gut and skin mucosal surfaces in yellowtail kingfish displaying signs of gut inflammation, as well as explored the host gene expression in these tissues in order to improve our understanding of the underlying mechanisms that contribute to the emergence of these conditions. For this, we obtained and analyzed 16S rDNA and transcriptomic (RNA-Seq) sequence data from the gut and skin mucosa of fish exhibiting different health states (i.e., healthy fish and fish at the early and late stages of enteritis). Both the gut and skin microbiota were perturbed by the disease. More specifically, the gastrointestinal microbiota of diseased fish was dominated by an uncultured Mycoplasmataceae sp., and fish at the early stage of the disease showed a significant loss of diversity in the skin. Using transcriptomics, we found that only a few genes were significantly differentially expressed in the gut. In contrast, gene expression in the skin differed widely between health states, in particular in the fish at the late stage of the disease. These changes were associated with several metabolic pathways that were differentially expressed and reflected a weakened host. Altogether, this study highlights the sensitivity of the skin mucosal surface in response to gut inflammation.
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Belső, Nóra. "New therapeutic strategies of lichen ruber planus." Bőrgyógyászati és Venerológiai Szemle 97, no. 5 (October 29, 2021): 278–82. http://dx.doi.org/10.7188/bvsz.2021.97.5.7.

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Lichen ruber planus/lichen planus (LP), is a chronic immune-mediated inflammatory disease that affects the skin, oral mucosa, genital mucosa, scalp and nails. Planar, purple, polygonal, pruritic, papules and plaques appear on the flexor surfaces of the wrists, forearms and legs. Mucosal lesions are often lacy, reticular, white lines known as Wickham striae. Topical corticosteroids are the first-line therapy for all forms of LP, for severe, widespread LP systemic corticosteroids, acitretine, oral immunosuppressants or narrowband UVB therapy should be considered. Cutaneous LP may resolve spontaneously within one or two years, while mucosal LP may be more persistent and resistant to treatment.
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34

Shrestha, Umid Kumar. "Immunology of the gut and oral tolerance." Journal of Advances in Internal Medicine 4, no. 1 (December 18, 2015): 16–24. http://dx.doi.org/10.3126/jaim.v4i1.14176.

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The pathogens and harmless antigens from the bacterial flora and food constantly expose the mucosal surface of the gastrointestinal tract. The mucosal epithelial cells act not only as a physical barrier, but also as a local immune system, which plays a vital role in defense and self-tolerance. The gut mucosal immune system comprises several compartments: Peyer’s patches and lymphoid follicles in the colonic mucosa, and lymphocytes in the lamina propria and intraepithelial lymphocytes. Peyer’s patches mediate antigen uptake via specialized epithelial cells (M cells) and are rich in B cells for class switching into IgA-secreting cells. IgA secretion is one of the primary defenses against pathogens at mucosal surfaces. The lamina propria contains a high proportion of activated and memory T cells that allows rapid immune response against pathogens. In the physiological situation, mucosally encountered antigens induce tolerance of lamina propria and intraepithelial lymphocytes by modified antigen presentation, antigen-induced anergy, or deletion of T cells, or regulation of effector T cells by regulatory or suppressor T cells. Costimulatory molecules mediate cellular interaction and induce regulatory cytokines. While the absence of gut immune privilege to food results in food allergy, the consequences of immune privilege collapse to commensal gut flora is Inflammatory Bowel Disease (IBD). Hence, the knowledge of the homeostatic regulation of the intestinal immune system paves the way for the development of the new immunomodulatory drugs in the therapy of IBD. Moreover, the generation of immune mediated cells through orally fed antigens could be the area of research in the treatment of certain autoimmune diseases.Journal of Advances in Internal Medicine 2015;04(01):16-24
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35

Chan, Hon Fai, Ruike Zhao, German A. Parada, Hu Meng, Kam W. Leong, Linda G. Griffith, and Xuanhe Zhao. "Folding artificial mucosa with cell-laden hydrogels guided by mechanics models." Proceedings of the National Academy of Sciences 115, no. 29 (July 2, 2018): 7503–8. http://dx.doi.org/10.1073/pnas.1802361115.

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The surfaces of many hollow or tubular tissues/organs in our respiratory, gastrointestinal, and urogenital tracts are covered by mucosa with folded patterns. The patterns are induced by mechanical instability of the mucosa under compression due to constrained growth. Recapitulating this folding process in vitro will facilitate the understanding and engineering of mucosa in various tissues/organs. However, scant attention has been paid to address the challenge of reproducing mucosal folding. Here we mimic the mucosal folding process using a cell-laden hydrogel film attached to a prestretched tough-hydrogel substrate. The cell-laden hydrogel constitutes a human epithelial cell lining on stromal component to recapitulate the physiological feature of a mucosa. Relaxation of the prestretched tough-hydrogel substrate applies compressive strains on the cell-laden hydrogel film, which undergoes mechanical instability and evolves into morphological patterns. We predict the conditions for mucosal folding as well as the morphology of and strain in the folded artificial mucosa using a combination of theory and simulation. The work not only provides a simple method to fold artificial mucosa but also demonstrates a paradigm in tissue engineering via harnessing mechanical instabilities guided by quantitative mechanics models.
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36

Schuppler, Markus, and Martin J. Loessner. "The Opportunistic PathogenListeria monocytogenes: Pathogenicity and Interaction with the Mucosal Immune System." International Journal of Inflammation 2010 (2010): 1–12. http://dx.doi.org/10.4061/2010/704321.

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Listeria monocytogenesis an opportunistic foodborne pathogen causing listeriosis, an often fatal infection leading to meningitis, sepsis, or infection of the fetus and abortion in susceptible individuals. It was recently found that the bacterium can also cause acute, self-limiting febrile gastroenteritis in healthy individuals. In the intestinal tract,L. monocytogenespenetrates the mucosa directly via enterocytes, or indirectly via invasion of Peyer’s patches. Animal models forL. monocytogenesinfection have provided many insights into the mechanisms of pathogenesis, and the development of new model systems has allowed the investigation of factors that influence adaptation to the gastrointestinal environment as well as adhesion to and invasion of the intestinal mucosa. The mucosal surfaces of the gastrointestinal tract are permanently exposed to an enormous antigenic load derived from the gastrointestinal microbiota present in the human bowel. The integrity of the important epithelial barrier is maintained by the mucosal immune system and its interaction with the commensal flora via pattern recognition receptors (PRRs). Here, we discuss recent advances in our understanding of the interaction ofL. monocytogeneswith the host immune system that triggers the antibacterial immune responses on the mucosal surfaces of the human gastrointestinal tract.
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Barker, Emilia, Lina AlQobaly, Zahab Shaikh, Kirsty Franklin, and Keyvan Moharamzadeh. "Implant Soft-Tissue Attachment Using 3D Oral Mucosal Models—A Pilot Study." Dentistry Journal 8, no. 3 (July 7, 2020): 72. http://dx.doi.org/10.3390/dj8030072.

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Purpose: The aim of this study was to investigate soft-tissue attachment to different metal, ceramic, and polymer implant surfaces using an inflamed, three-dimensional (3D), tissue-engineered, human oral mucosal model, as well as multiple-endpoint qualitative and quantitative biological approaches. Methods: Normal human oral fibroblasts, OKF6/TERT-2 keratinocytes and THP-1 monocytes were cultured, and full-thickness, 3D oral mucosal models were engineered inside tissue culture inserts. Sand-blasted and acid-etched (SLA) and machined (M) titanium–zirconium alloy (TiZr; commercially known as Roxolid; Institut Straumann AG, Switzerland), ceramic (ZrO2), and polyether ether ketone (PEEK) rods (Ø 4 mm × 8 mm) were inserted into the center of tissue-engineered oral mucosa following a Ø 4mm punch biopsy. Inflammation was simulated with addition of the lipopolysaccharide (LPS) of Escherichia coli (E. coli) and tumor necrosis factor (TNF)-alpha to the culture medium. Implant soft-tissue attachment was assessed using histology, an implant pull-test with PrestoBlue assay, and scanning electron microscopy (SEM). Results: Inflamed, full-thickness, 3D human oral mucosal models with inserted implants were successfully engineered and histologically characterized. The implant pull-test with PrestoBlue assay showed higher viability of the tissue that remained attached to the TiZr-SLA surface compared to the other test groups. This difference was statistically significant (p < 0.05). SEM analysis showed evidence of epithelial cell attachment on different implant surfaces. Conclusions: The inflamed, 3D, oral mucosal model has the potential to be used as a suitable in vitro test system for visualization and quantification of implant soft-tissue attachment. The results of our study indicate greater soft tissue attachment to TiZr-SLA compared to TiZr-M, ceramic, and PEEK surfaces.
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Hu, Jinjie, Murray B. Gardner, and Christopher J. Miller. "Simian Immunodeficiency Virus Rapidly Penetrates the Cervicovaginal Mucosa after Intravaginal Inoculation and Infects Intraepithelial Dendritic Cells." Journal of Virology 74, no. 13 (July 1, 2000): 6087–95. http://dx.doi.org/10.1128/jvi.74.13.6087-6095.2000.

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ABSTRACT Despite recent insights into mucosal human immunodeficiency virus (HIV) transmission, the route used by primate lentiviruses to traverse the stratified squamous epithelium of mucosal surfaces remains undefined. To determine if dendritic cells (DC) are used by primate lentiviruses to traverse the epithelial barrier of the genital tract, rhesus macaques were intravaginally exposed to cell-free simian immunodeficiency virus SIVmac251. We examined formalin-fixed tissues and HLA-DR+-enriched cell suspensions to identify the cells containing SIV RNA in the genital tract and draining lymph nodes within the first 24 h of infection. Using SIV-specific fluorescent in situ hybridization combined with immunofluorescent antibody labeling of lineage-specific cell markers, numerous SIV RNA+ DC were documented in cell suspensions from the vaginal epithelium 18 h after vaginal inoculation. In addition, we determined the minimum time that the SIV inoculum must remain in contact with the genital mucosa for the virus to move from the vaginal lumen into the mucosa. We now show that SIV enters the vaginal mucosa within 60 min of intravaginal exposure, infecting primarily intraepithelial DC and that SIV-infected cells are located in draining lymph nodes within 18 h of intravaginal SIV exposure. The speed with which primate lentiviruses penetrate mucosal surfaces, infect DC, and disseminate to draining lymph nodes poses a serious challenge to HIV vaccine development.
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39

Lambeth, Christopher, Jason Amatoury, Ziyu Wang, Sheryl Foster, Terence Amis, and Kristina Kairaitis. "Velopharyngeal mucosal surface topography in healthy subjects and subjects with obstructive sleep apnea." Journal of Applied Physiology 122, no. 3 (March 1, 2017): 482–91. http://dx.doi.org/10.1152/japplphysiol.00764.2016.

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Macroscopic pharyngeal anatomical abnormalities are thought to contribute to the pathogenesis of upper airway (UA) obstruction in obstructive sleep apnea (OSA). Microscopic changes in the UA mucosal lining of OSA subjects are reported; however, the impact of these changes on UA mucosal surface topography is unknown. This study aimed to 1) develop methodology to measure UA mucosal surface topography, and 2) compare findings from healthy and OSA subjects. Ten healthy and eleven OSA subjects were studied. Awake, gated (end expiration), head and neck position controlled magnetic resonance images (MRIs) of the velopharynx (VP) were obtained. VP mucosal surfaces were segmented from axial images, and three-dimensional VP mucosal surface models were constructed. Curvature analysis of the models was used to study the VP mucosal surface topography. Principal, mean, and Gaussian curvatures were used to define surface shape composition and surface roughness of the VP mucosal surface models. Significant differences were found in the surface shape composition, with more saddle/spherical and less flat/cylindrical shapes in OSA than healthy VP mucosal surface models ( P < 0.01). OSA VP mucosal surface models were also found to have more mucosal surface roughness ( P < 0.0001) than healthy VP mucosal surface models. Our novel methodology was utilized to model the VP mucosal surface of OSA and healthy subjects. OSA subjects were found to have different VP mucosal surface topography, composed of increased irregular shapes and increased roughness. We speculate increased irregularity in VP mucosal surface may increase pharyngeal collapsibility as a consequence of friction-related pressure loss. NEW & NOTEWORTHY A new methodology was used to model the upper airway mucosal surface topography from magnetic resonance images of patients with obstructive sleep apnea and healthy adults. Curvature analysis was used to analyze the topography of the models, and a new metric was derived to describe the mucosal surface roughness. Increased roughness was found in the obstructive sleep apnea vs. healthy group, but further research is required to determine the functional effects of the measured difference on upper airway airflow mechanics.
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40

Hellfritzsch and Scherließ. "Mucosal Vaccination via the Respiratory Tract." Pharmaceutics 11, no. 8 (August 1, 2019): 375. http://dx.doi.org/10.3390/pharmaceutics11080375.

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Vaccine delivery via mucosal surfaces is an interesting alternative to parenteral vaccine administration, as it avoids the use of a needle and syringe. Mucosal vaccine administration also targets the mucosal immune system, which is the largest lymphoid tissue in the human body. The mucosal immune response involves systemic, antigen-specific humoral and cellular immune response in addition to a local response which is characterised by a predominantly cytotoxic T cell response in combination with secreted IgA. This antibody facilitates pathogen recognition and deletion prior to entrance into the body. Hence, administration via the respiratory mucosa can be favoured for all pathogens which use the respiratory tract as entry to the body, such as influenza and for all diseases directly affecting the respiratory tract such as pneumonia. Additionally, the different mucosal tissues of the human body are interconnected via the so-called “common mucosal immune system”, which allows induction of an antigen-specific immune response in distant mucosal sites. Finally, mucosal administration is also interesting in the area of therapeutic vaccination, in which a predominant cellular immune response is required, as this can efficiently be induced by this route of delivery. The review gives an introduction to respiratory vaccination, formulation approaches and application strategies.
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41

Southern, Peter, Julie Horbul, Diane Maher, and Dana A. Davis. "C. albicans Colonization of Human Mucosal Surfaces." PLoS ONE 3, no. 4 (April 30, 2008): e2067. http://dx.doi.org/10.1371/journal.pone.0002067.

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42

MAYER, LLOYD. "Innate and Acquired Immunity at Mucosal Surfaces." Viral Immunology 13, no. 4 (December 2000): 477–80. http://dx.doi.org/10.1089/vim.2000.13.477.

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43

Matarazzo, F., A. C. Ribeiro, M. Faveri, C. Taddei, M. B. Martinez, and M. P. A. Mayer. "The domain Archaea in human mucosal surfaces." Clinical Microbiology and Infection 18, no. 9 (September 2012): 834–40. http://dx.doi.org/10.1111/j.1469-0691.2012.03958.x.

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44

Sheldrake, Richard F., and Alan J. Husband. "Immune defences at mucosal surfaces in ruminants." Journal of Dairy Research 52, no. 4 (November 1985): 599–613. http://dx.doi.org/10.1017/s0022029900024560.

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45

Levine, Myron M., and Gordon Dougan. "Optimism over vaccines administered via mucosal surfaces." Lancet 351, no. 9113 (May 1998): 1375–76. http://dx.doi.org/10.1016/s0140-6736(05)79439-3.

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46

Fagarasan, Sidonia, and Tasuku Honjo. "Regulation of IgA synthesis at mucosal surfaces." Current Opinion in Immunology 16, no. 3 (June 2004): 277–83. http://dx.doi.org/10.1016/j.coi.2004.03.005.

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47

McNeilly, Celia L., Michael L. Crichton, Clare A. Primiero, Ian H. Frazer, Michael S. Roberts, and Mark A. F. Kendall. "Microprojection arrays to immunise at mucosal surfaces." Journal of Controlled Release 196 (December 2014): 252–60. http://dx.doi.org/10.1016/j.jconrel.2014.09.028.

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48

Gerstner, Andreas O. H., Wiebke Laffers, Friedrich Bootz, Daniel L. Farkas, Ron Martin, Jörg Bendix, and Boris Thies. "Hyperspectral imaging of mucosal surfaces in patients." Journal of Biophotonics 5, no. 3 (January 9, 2012): 255–62. http://dx.doi.org/10.1002/jbio.201100081.

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49

Moyes, David L., and Julian R. Naglik. "Mucosal Immunity andCandida albicansInfection." Clinical and Developmental Immunology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/346307.

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Interactions between mucosal surfaces and microbial microbiota are key to host defense, health, and disease. These surfaces are exposed to high numbers of microbes and must be capable of distinguishing between those that are beneficial or avirulent and those that will invade and cause disease. Our understanding of the mechanisms involved in these discriminatory processes has recently begun to expand as new studies bring to light the importance of epithelial cells and novel immune cell subsets such as Th17 T cells in these processes. Elucidating how these mechanisms function will improve our understanding of many diverse diseases and improve our ability to treat patients suffering from these conditions. In our voyage to discover these mechanisms, mucosal interactions with opportunistic commensal organisms such as the fungusCandida albicansprovide insights that are invaluable. Here, we review current knowledge of the interactions betweenC. albicansand epithelial surfaces and how this may shape our understanding of microbial-mucosal interactions.
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Connell, Hugh, Maria Hedlund, William Agace, and Catharina Svanborg. "Bacterial Attachment To Uro-Epithelial Cells: Mechanisms and Consequences." Advances in Dental Research 11, no. 1 (April 1997): 50–58. http://dx.doi.org/10.1177/08959374970110011701.

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Microbial attachment to mucosal surfaces is a first step in mucosal infection. Specific interactions between microbial surface ligands and host receptors influence the distribution of microbes in their sites of infection. Adhesion has often been regarded as a sufficient end point, explaining tissue tropism and bacterial persistence at mucosal sites. Adherence, however, is also a virulence factor through which microbes gain access to host tissues, upset the integrity of the mucosal barrier, and cause disease. The induction of mucosal inflammation is one aspect of this process. Bacterial attachment to mucosal surfaces activates the production of pro-inflammatory cytokines that cause both local and systemic inflammation. Epithelial cells are one source of these cytokines. The binding of fimbrial lectins to epithelial cell receptors triggers transmembrane signaling events that upregulate cytokine-specific mRNA and increase cytokine secretion. P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response. Spread of cytokines and other pro-inflammatory mediators from the local site contributes to the symptoms and signs of infection.
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