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Journal articles on the topic 'Mucosal immunity'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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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

Mayer, Lloyd. "Mucosal Immunity." Pediatrics 111, Supplement_3 (June 1, 2003): 1595–600. http://dx.doi.org/10.1542/peds.111.s3.1595.

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Food allergy is the manifestation of an abnormal immune response to antigen delivered by the oral route. Normal mucosal immune responses are generally associated with suppression of immunity. A normal mucosal immune response relies heavily on a number of factors: strong physical barriers, luminal digestion of potential antigens, selective antigen sampling sites, and unique T-cell subpopulations that effect suppression. In the newborn, several of these pathways are not matured, allowing for sensitization rather than suppression. With age, the mucosa associated lymphoid tissue matures, and in most individuals this allows for generation of the normal suppressed tone of the mucosa associated lymphoid tissue. As a consequence, food allergies are largely outgrown. This article deals with the normal facets of mucosal immune responses and postulates how the different processes may be defective in food-allergic patients.

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3

Yasui, Hisako. "Mucosal Immunity/Mucosal Vaccine." Nippon Shokuhin Kagaku Kogaku Kaishi 56, no. 3 (2009): 191. http://dx.doi.org/10.3136/nskkk.56.191.

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4

van Oss, Carel J. "Mucosal Immunity." Immunological Investigations 14, no. 3 (January 1985): 279. http://dx.doi.org/10.3109/08820138509076154.

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5

NAGURA, HIROSHI. "Mucosal immunity." Nihon Naika Gakkai Zasshi 84, no. 4 (1995): 632–39. http://dx.doi.org/10.2169/naika.84.632.

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6

Dwinell, Michael B., and Martin F. Kagnoff. "Mucosal immunity." Current Opinion in Gastroenterology 15, no. 1 (January 1999): 33. http://dx.doi.org/10.1097/00001574-199901000-00007.

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7

Mayer, Lloyd. "Mucosal immunity." Immunological Reviews 206, no. 1 (August 2005): 5. http://dx.doi.org/10.1111/j.0105-2896.2005.00296.x.

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8

Petzoldt, Klaus. "Mucosal immunity." Veterinary Immunology and Immunopathology 35 (February 1993): 40–48. http://dx.doi.org/10.1016/0165-2427(93)90134-p.

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9

Lü, F. X., and R. S. Jacobson. "Oral Mucosal Immunity and HIV/SIV Infection." Journal of Dental Research 86, no. 3 (March 2007): 216–26. http://dx.doi.org/10.1177/154405910708600305.

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Human Immunodeficiency Virus (HIV) transmission through genital and rectal mucosa has led to intensive study of mucosal immune responses to HIV and to the development of a vaccine administered locally. However, HIV transmission through the oral mucosa is a rare event. The oral mucosa represents a physical barrier and contains immunological elements to prevent the invasion of pathogenic organisms. This particular defense differs between micro-compartments represented by the salivary glands, oral mucosa, and palatine tonsils. Secretory immunity of the salivary glands, unique features of cellular structure in the oral mucosa and palatine tonsils, the high rate of oral blood flow, and innate factors in saliva may all contribute to the resistance to HIV/Simian Immunodeficiency Virus (SIV) oral mucosal infection. In the early stage of HIV infection, humoral and cellular immunity and innate immune functions in oral mucosa are maintained. However, these particular immune responses may all be impaired as a result of chronic HIV infection. A better understanding of oral mucosal immune mechanisms should lead to improved prevention of viral and bacterial infections, particularly in immunocompromised persons with Acquired Immune Deficiency Syndrome (AIDS), and to the development of a novel strategy for a mucosal AIDS vaccine, as well as vaccines to combat other oral diseases, such as dental caries and periodontal diseases.

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10

Nie, Siru, and Yuan Yuan. "The Role of Gastric Mucosal Immunity in Gastric Diseases." Journal of Immunology Research 2020 (July 24, 2020): 1–8. http://dx.doi.org/10.1155/2020/7927054.

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Gastric mucosa plays its immune function through innate and adaptive immunity by recruiting immune cells and releasing corresponding cytokines, which have an inseparable relationship with gastric diseases. Whether infective gastric diseases caused by Helicobacter pylori, Epstein-Barr virus or other microbe, noninfective gastric diseases, or gastric cancer, gastric mucosal immunity plays an important role in the occurrence and development of the disease. Understanding the unique immune-related tissue structure of the gastric mucosa and its role in immune responses can help prevent gastric diseases or treat them through immunotherapy. In this review, we summarize the basic feature of gastric mucosal immunity and its relationship with gastric diseases to track the latest progress of gastric mucosal immunity, update relevant knowledge and provide theoretical reference for the prevention and treatment of gastric diseases based on the gastric mucosal immunity.

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11

Loehr, B. I., P. Willson, L. A. Babiuk, and S. van Drunen Littel-van den Hurk. "Gene Gun-Mediated DNA Immunization Primes Development of Mucosal Immunity against Bovine Herpesvirus 1 in Cattle." Journal of Virology 74, no. 13 (July 1, 2000): 6077–86. http://dx.doi.org/10.1128/jvi.74.13.6077-6086.2000.

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ABSTRACT Vaccination by a mucosal route is an excellent approach to the control of mucosally acquired infections. Several reports on rodents suggest that DNA vaccines can be used to achieve mucosal immunity when applied to mucosal tissues. However, with the exception of one study with pigs and another with horses, there is no information on mucosal DNA immunization of the natural host. In this study, the potential of inducing mucosal immunity in cattle by immunization with a DNA vaccine was demonstrated. Cattle were immunized with a plasmid encoding bovine herpesvirus 1 (BHV-1) glycoprotein B, which was delivered with a gene gun either intradermally or intravulvomucosally. Intravulvomucosal DNA immunization induced strong cellular immune responses and primed humoral immune responses. This was evident after BHV-1 challenge when high levels of both immunoglobulin G (IgG) and IgA were detected. Intradermal delivery resulted in lower levels of immunity than mucosal immunization. To determine whether the differences between the immune responses induced by intravulvomucosal and intradermal immunizations might be due to the efficacy of antigen presentation, the distributions of antigen and Langerhans cells in the skin and mucosa were compared. After intravulvomucosal delivery, antigen was expressed early and throughout the mucosa, but after intradermal administration, antigen expression occurred later and superficially in the skin. Furthermore, Langerhans cells were widely distributed in the mucosal epithelium but found primarily in the basal layers of the epidermis of the skin. Collectively, these observations may account for the stronger immune response induced by mucosal administration.

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12

Li, Wu, Guangcun Deng, Min Li, Xiaoming Liu, and Yujiong Wang. "Roles of Mucosal Immunity againstMycobacterium tuberculosisInfection." Tuberculosis Research and Treatment 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/791728.

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Mycobacterium tuberculosis(Mtb), the causative agent of tuberculosis (TB), is one of the world's leading infectious causes of morbidity and mortality. As a mucosal-transmitted pathogen, Mtb infects humans and animals mainly through the mucosal tissue of the respiratory tract. Apart from providing a physical barrier against the invasion of pathogen, the major function of the respiratory mucosa may be to serve as the inductive sites to initiate mucosal immune responses and sequentially provide the first line of defense for the host to defend against this pathogen. A large body of studies in the animals and humans have demonstrated that the mucosal immune system, rather than the systemic immune system, plays fundamental roles in the host’s defense against Mtb infection. Therefore, the development of new vaccines and novel delivery routes capable of directly inducing respiratory mucosal immunity is emphasized for achieving enhanced protection from Mtb infection. In this paper, we outline the current state of knowledge regarding the mucosal immunity against Mtb infection, including the development of TB vaccines, and respiratory delivery routes to enhance mucosal immunity are discussed.

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13

Lencer, Wayne I., and Ulrich H. von Andrian. "Eliciting Mucosal Immunity." New England Journal of Medicine 365, no. 12 (September 22, 2011): 1151–53. http://dx.doi.org/10.1056/nejmcibr1107816.

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14

Scanlon, Seth Thomas. "Mechanosensing mucosal immunity." Science 366, no. 6466 (November 7, 2019): 703.2–704. http://dx.doi.org/10.1126/science.366.6466.703-b.

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15

Feller, L., M. Altini, R. A. G. Khammissa, R. Chandran, M. Bouckaert, and J. Lemmer. "Oral mucosal immunity." Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology 116, no. 5 (November 2013): 576–83. http://dx.doi.org/10.1016/j.oooo.2013.07.013.

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16

Chang, Sun-Young, Hyun-Jeong Ko, and Mi-Na Kweon. "Mucosal dendritic cells shape mucosal immunity." Experimental & Molecular Medicine 46, no. 3 (March 2014): e84-e84. http://dx.doi.org/10.1038/emm.2014.16.

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17

Weinberg, A., J. R. Naglik, A. Kohli, S. M. Tugizov, P. L. Fidel, Y. Liu, and M. Herzberg. "Innate Immunity Including Epithelial and Nonspecific Host Factors." Advances in Dental Research 23, no. 1 (March 25, 2011): 122–29. http://dx.doi.org/10.1177/0022034511399917.

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The majority of HIV infections are initiated at mucosal sites. The oral mucosal tissue has been shown to be a potential route of entry in humans and primates. Whereas HIV RNA, proviral DNA, and infected cells are detected in the oral mucosa and saliva of infected individuals, it appears that the oral mucosa is not permissive for efficient HIV replication and therefore may differ in susceptibility to infection when compared to other mucosal sites. Since there is no definitive information regarding the fate of the HIV virion in mucosal epithelium, there is a pressing need to understand what occurs when the virus is in contact with this tissue, what mechanisms are in play to determine the outcome, and to what degree the mechanisms and outcomes differ between mucosal sites. Workshop 1B tackled 5 important questions to define current knowledge about epithelial cell-derived innate immune agents, commensal and endogenous pathogens, and epithelial cells and cells of the adaptive immune system and how they contribute to dissemination or resistance to HIV infection. Discovering factors that explain the differential susceptibility and resistance to HIV infection in mucosal sites will allow for the identification and development of novel protective strategies.

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18

Fantry, George T., and Stephen P. James. "Cell-mediated immunity and mucosal immunity." Current Opinion in Gastroenterology 10, no. 4 (July 1994): 365–73. http://dx.doi.org/10.1097/00001574-199407000-00003.

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19

Challacombe, S. J., P. L. Fidel, S. Tugizov, L. Tao, and S. M. Wahl. "HIV Infection and Specific Mucosal Immunity." Advances in Dental Research 23, no. 1 (March 25, 2011): 142–51. http://dx.doi.org/10.1177/0022034511400222.

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Most HIV infections are transmitted across mucosal epithelium. An area of fundamental importance is understanding the role of innate and specific mucosal immunity in susceptibility or protection against HIV infection, as well as the effect of HIV infection on mucosal immunity, which leads to increased susceptibility to bacterial, fungal, and viral infections of oral and other mucosae. This workshop attempted to address 5 basic issues—namely, HIV acquisition across mucosal surfaces, innate and adaptive immunity in HIV resistance, antiviral activity of breast milk as a model mucosal fluid, neutralizing immunoglobulin A antibodies against HIV, and progress toward a mucosal vaccine against HIV. The workshop attendants agreed that progress had been made in each area covered, with much recent information. However, these advances revealed how little work had been performed on stratified squamous epithelium compared with columnar epithelium, and the attendants identified several important biological questions that had not been addressed. It is increasingly clear that innate immunity has an important biological role, although basic understanding of the mechanisms of normal homeostasis is still being investigated. Application of the emerging knowledge was lacking with regard to homeostatic mucosal immunity to HIV and its role in changing this homeostasis. With regard to breast milk, a series of studies have demonstrated the differences between transmitters and nontransmitters, although whether these findings could be generalized to other secretions such as saliva was less clear. Important progress toward an oral mucosal HIV vaccine has been made, demonstrating proof of principle for administering vaccine candidates into oral lymphoid tissues to trigger anti-HIV local and systemic immune responses. Similarly, experimental data emphasized the central role of neutralizing antibodies to prevent HIV infection via mucosal routes.

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20

Sowell, Ryan, Magdalena Rogozinska, Christine Nelson, Vaiva Vezys, and Amanda Marzo. "mTOR-dependent regulation of mucosal CD8 T cell immunity (P3221)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 171.23. http://dx.doi.org/10.4049/jimmunol.190.supp.171.23.

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Abstract Mucosal tissues are sites of frequent pathogen exposure and major routes for the transmission of infectious diseases. Migration of virus-specific memory CD8 T cells into mucosal tissues such as the small intestine and vaginal mucosa is highly restricted to non-circulating tissue resident memory CD8 T cells. Resident mucosal memory CD8 T cells are sufficient to protect against the establishment of mucosa-acquired viral infections, and thus it is essential to develop vaccine strategies that elicit long-lived mucosal CD8 T cells. CD8 T cells residing in mucosal tissues are phenotypically distinct from those in secondary lymphoid tissues and factors critical for their formation are poorly defined. It is also unclear whether mucosal CD8 T cells possess a unique requirement for their generation and maintenance from that of circulating memory CD8 T cells. We report that unlike in the secondary lymphoid tissues, the formation of virus-specific memory CD8 T cells in the small intestine and vaginal mucosa is dependent on mTOR signaling. In addition, we demonstrate using a CD8 T cell mediated model of intestinal autoimmune disease that inhibiting mTOR results in a loss of CD8 T cells in the small intestine and protects mice from lethality. Furthermore, we will discuss data that targets mTOR signaling intrinsically within the CD8 T cells to provide mechanistic insight into how the mTOR pathway specifically controls the generation of mucosal CD8 T cells in response to viral infections.

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21

Strbo, Natasa, Savita Pahwa, Michael Kolber, and Eckhard Podack. "Induction of mucosal immunity by hsp gp96 (41.2)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S30. http://dx.doi.org/10.4049/jimmunol.178.supp.41.2.

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Abstract Targeting immune responses to the mucosal entry site before pathogen dissemination is critical for protection. We have generated a secreted gp96-fusion protein (gp96-Ig) that mediated strong, antigen specific CD8-CTL expansion in vivo. The aim of this study was to evaluate the effect of the site of gp96 secretion on mucosal immunity. Expansion and migration of antigen specific CD8 T cells (adoptively transferred gfp-OT-I responder cells) were measured in response to immunization. Following different routes of administration of gp96-Ig secreting cells (EG7/3T3-OVA) the OT-I response was measured in the peritoneal cavity, spleen, mesenteric lymph nodes and gut mucosa. OT-I home significantly more efficiently to the gut mucosa if the gp96-Ig was delivered by the intraperitoneal route. Vaginal administration of gp96 also mediated mucosal immunity while subcutaneous and intradermal immunization delivered the weakest response. Secreted gp96-ova complexes recruited OT-I to Peyer’s Patches, intraepithelial compartment and lamina propria within five days. Mucosal OT-I express alpha4beta7, alphaEbeta7/CD103, CCR9, granzyme B, IFNgamma and exhibited effector memory phenotype. Our results indicate that peritoneally or vaginally cell secreted gp96-Ig induces migration of effector memory cells equipped with cytotoxic molecules into the mucosal compartment by inducing selective expression of gut-homing markers.

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22

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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23

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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24

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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25

Wyatt, Carol R. "Cryptosporidium parvumand mucosal immunity in neonatal cattle." Animal Health Research Reviews 1, no. 1 (June 2000): 25–34. http://dx.doi.org/10.1017/s1466252300000037.

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AbstractCryptosporidium parvumis an important zoonotic protozoan pathogen that causes acute infection and self-limiting gastrointestinal disease in neonatal calves. There are currently no consistently effective antimicrobials available to control cryptosporidiosis. Therefore, immunotherapeutic and vaccination protocols offer the greatest potential for long-term control of the disease. In order to devise effective control measures, it is important to better define mucosal immunity toC. parvumin young calves. This review summarizes the information that has accumulated over the last decade which helps to define the intestinal mucosal immune system in neonatal calves, and the events that occur in the intestinal mucosa after infection byC. parvum.

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26

Ogra, Pearay L., Hiromasa Okayasu, Cecil Czerkinsky, and Roland W. Sutter. "Mucosal immunity to poliovirus." Expert Review of Vaccines 10, no. 10 (October 2011): 1389–92. http://dx.doi.org/10.1586/erv.11.106.

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27

Elson, Charles O. "Advances in Mucosal Immunity." Drugs 54, Supplement 1 (1997): 13–14. http://dx.doi.org/10.2165/00003495-199700541-00005.

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28

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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29

CHALLACOMBE, S. J. "Assessing mucosal humoral immunity." Clinical & Experimental Immunology 100, no. 2 (June 28, 2008): 181–82. http://dx.doi.org/10.1111/j.1365-2249.1995.tb03649.x.

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30

Bamias, Giorgos, Kristen O. Arseneau, and Fabio Cominelli. "Cytokines and mucosal immunity." Current Opinion in Gastroenterology 30, no. 6 (November 2014): 547–52. http://dx.doi.org/10.1097/mog.0000000000000118.

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31

Kawauchi, H., K. Sano, and R. Ishimitsu. "Mucosal Immunity of Nasopharynx." Nihon Bika Gakkai Kaishi (Japanese Journal of Rhinology) 36, no. 2 (1997): 150–54. http://dx.doi.org/10.7248/jjrhi1982.36.2_150.

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32

Zeissig, Sebastian, and Richard S. Blumberg. "Immunity Against Mucosal Pathogens." Gastroenterology 137, no. 4 (October 2009): 1533. http://dx.doi.org/10.1053/j.gastro.2009.08.037.

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33

Holmgren, Jan, and Cecil Czerkinsky. "Mucosal immunity and vaccines." Nature Medicine 11, S4 (April 2005): S45—S53. http://dx.doi.org/10.1038/nm1213.

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34

Holmgren, Jan. "Mucosal immunity and vaccination." FEMS Microbiology Letters 89, no. 1 (December 1991): 1–10. http://dx.doi.org/10.1111/j.1574-6968.1991.tb04964.x.

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35

Schulthess, J., D. Fourreau, S. Darche, B. Meresse, L. Kasper, N. Cerf-Bensussan, and D. Buzoni-Gatel. "Mucosal immunity inToxoplasma gondiiinfection." Parasite 15, no. 3 (September 2008): 389–95. http://dx.doi.org/10.1051/parasite/2008153389.

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36

Monteleone, Giovanni, Ilaria Peluso, Daniele Fina, Roberta Caruso, Fabio Andrei, Claudio Tosti, and Francesco Pallone. "Bacteria and mucosal immunity." Digestive and Liver Disease 38 (December 2006): S256—S260. http://dx.doi.org/10.1016/s1590-8658(07)60005-x.

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37

Mannick, Elizabeth, and John N. Udall. "Neonatal Gastrointestinal Mucosal Immunity." Clinics in Perinatology 23, no. 2 (June 1996): 287–304. http://dx.doi.org/10.1016/s0095-5108(18)30243-4.

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38

O'Hagan, D. T. "HIV and mucosal immunity." Lancet 337, no. 8752 (May 1991): 1289. http://dx.doi.org/10.1016/0140-6736(91)92958-5.

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39

WERSHIL, B., and G. FURUTA. "4. Gastrointestinal mucosal immunity." Journal of Allergy and Clinical Immunology 121, no. 2 (February 2008): S380—S383. http://dx.doi.org/10.1016/j.jaci.2007.10.023.

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40

Kyd, Jennelle. "Immunity against mucosal pathogens." Human Vaccines 6, no. 3 (March 2010): 235–36. http://dx.doi.org/10.4161/hv.6.3.10016.

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41

Mackey-Lawrence, N. M., and W. A. Petri. "Leptin and mucosal immunity." Mucosal Immunology 5, no. 5 (June 13, 2012): 472–79. http://dx.doi.org/10.1038/mi.2012.40.

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42

Brandtzaeg, P. "Homeostatic impact of indigenous microbiota and secretory immunity." Beneficial Microbes 1, no. 3 (September 1, 2010): 211–27. http://dx.doi.org/10.3920/bm2010.0009.

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In the process of evolution, the mucosal immune system has generated two layers of anti-inflammatory defence: (1) immune exclusion performed by secretory IgA (and secretory IgM) antibodies to modulate or inhibit surface colonisation of microorganisms and dampen penetration of potentially dangerous antigens; and (2) suppressive mechanisms to avoid local and peripheral hypersensitivity to innocuous antigens, particularly food proteins and components of commensal bacteria. When induced via the gut, the latter phenomenon is called 'oral tolerance', which mainly depends on the development of regulatory T (Treg) cells in mesenteric lymph nodes to which mucosal dendritic cells (DCs) carry exogenous antigens and become conditioned for induction of Treg cells. Mucosally induced tolerance appears to be a rather robust adaptive immune function in view of the fact that large amounts of food proteins pass through the gut, while overt and persistent food allergy is not so common. DCs are 'decision makers' in the immune system when they perform their antigen-presenting function, thus linking innate and adaptive immunity by sensing the exogenous mucosal impact (e.g. conserved microbial molecular patterns). A balanced indigenous microbiota is required to drive the normal development of both mucosa-associated lymphoid tissue, the epithelial barrier with its secretory IgA (and IgM) system, and mucosally induced tolerance mechanisms including the generation of Treg cells. Notably, polymeric Ig receptor (pIgR/SC) knock-out mice that lack secretory IgA and IgM antibodies show reduced epithelial barrier function and increased uptake of antigens from food and commensal bacteria. They therefore have a hyper-reactive immune system and show predisposition for systemic anaphylaxis after sensitisation; but this development is counteracted by enhanced oral tolerance induction as a homeostatic back-up mechanism.

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43

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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44

Hoft, Daniel F., and Chris S. Eickhoff. "Type 1 Immunity Provides Both Optimal Mucosal and Systemic Protection against a Mucosally Invasive, Intracellular Pathogen." Infection and Immunity 73, no. 8 (August 2005): 4934–40. http://dx.doi.org/10.1128/iai.73.8.4934-4940.2005.

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ABSTRACT It has been hypothesized that optimal vaccine immunity against mucosally invasive, intracellular pathogens may require the induction of different types of immune responses in mucosal and systemic lymphoid tissues. Mucosal type 2/3 responses (producing interleukin-4 [IL-4], IL-6 and/or transforming growth factor β) could be necessary for optimal induction of protective secretory immunoglobulin A responses. On the other hand, systemic type 1 responses (including gamma interferon [IFN-γ], tumor necrosis factor alpha, and optimal cytotoxic T-cell responses) are likely to be critical for protection against the disseminated intracellular replication that occurs after mucosal invasion. Despite these predictions, we recently found that vaccines inducing highly polarized type 1 immunity in both mucosal and systemic tissues provided optimal mucosal and systemic protection against the protozoan pathogen Trypanosoma cruzi. To further address this important question in a second model system, we now have studied the capacity of knockout mice to develop protective immune memory. T. cruzi infection followed by nifurtimox treatment rescue was used to immunize CD4, CD8, β2-microglobulin, inducible nitric oxide synthase (iNOS), IL-12, IFN-γ, and IL-4 knockout mice. Despite the previously demonstrated importance of CD4+ T cells, CD8+ T cells, and nitric oxide for T. cruzi immunity, CD4, CD8, and iNOS knockout mice developed mucosal and systemic protective immunity. However, IL-12, IFN-γ, and β2-microglobulin-deficient mice failed to develop mucosal or systemic protection. In contrast, IL-4 knockout mice developed maximal levels of both mucosal and systemic immune protection. These results strongly confirm our earlier conclusion from studies with polarizing vaccination protocols that type 1 immunity provides optimal mucosal and systemic protection against a mucosally invasive, intracellular pathogen.

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Clinton, Njinju Asaba, Sodiq Ayobami Hameed, Eugene Kusi Agyei, Joy Chinwendu Jacob, Victor Oyewale Oyebanji, and Cyril Ekabe Jabea. "Crosstalk between the Intestinal Virome and Other Components of the Microbiota, and Its Effect on Intestinal Mucosal Response and Diseases." Journal of Immunology Research 2022 (September 27, 2022): 1–23. http://dx.doi.org/10.1155/2022/7883945.

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In recent years, there has been ample evidence illustrating the effect of microbiota on gut immunity, homeostasis, and disease. Most of these studies have engaged more efforts in understanding the role of the bacteriome in gut mucosal immunity and disease. However, studies on the virome and its influence on gut mucosal immunity and pathology are still at infancy owing to limited metagenomic tools. Nonetheless, the existing studies on the virome have largely been focused on the bacteriophages as these represent the main component of the virome with little information on endogenous retroviruses (ERVs) and eukaryotic viruses. In this review, we describe the gut virome, and its role in gut mucosal response and disease progression. We also explore the crosstalk between the virome and other microorganisms in the gut mucosa and elaborate on how these interactions shape the gut mucosal immunity going from bacteriophages through ERVs to eukaryotic viruses. Finally, we elucidate the potential contribution of this crosstalk in the pathogenesis of inflammatory bowel diseases and colon cancer.

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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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Zainutdinov, S. S., G. F. Sivolobova, V. B. Loktev, and G. V. Kochneva. "Mucosal immunity and vaccines against viral infections." Problems of Virology 66, no. 6 (January 8, 2022): 399–408. http://dx.doi.org/10.36233/0507-4088-82.

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Mucosal immunity is realized through a structural and functional system called mucose-associated lymphoid tissue (MALT). MALT is subdivided into parts (clusters) depending on their anatomical location, but they all have a similar structure: mucus layer, epithelial tissue, lamina propria and lymphoid follicles. Plasma cells of MALT produce a unique type of immunoglobulins, IgA, which have the ability to polymerize. In mucosal immunization, the predominant form of IgA is a secretory dimer, sIgA, which is concentrated in large quantities in the mucosa. Mucosal IgA acts as a first line of defense and neutralizes viruses efficiently at the portal of entry, preventing infection of epithelial cells and generalization of infection. To date, several mucosal antiviral vaccines have been licensed, which include attenuated strains of the corresponding viruses: poliomyelitis, influenza, and rotavirus. Despite the tremendous success of these vaccines, in particular, in the eradication of poliomyelitis, significant disadvantages of using attenuated viral strains in their composition are the risk of reactogenicity and the possibility of reversion to a virulent strain during vaccination. Nevertheless, it is mucosal vaccination, which mimics a natural infection, is able to induce a fast and effective immune response and thus help prevent and possibly stop outbreaks of many viral infections. Currently, a number of intranasal vaccines based on a new vector approach are successfully undergoing clinical trials. In these vaccines, the safe viral vectors are used to deliver protectively significant immunogens of pathogenic viruses. The most tested vector for intranasal vaccines is adenovirus, and the most significant immunogen is SARSCoV-2 S protein. Mucosal vector vaccines against human respiratory syncytial virus and human immunodeficiency virus type 1 based on Sendai virus, which is able to replicate asymptomatically in cells of bronchial epithelium, are also being investigated.

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Jones-Carson, J., F. A. Vazquez-Torres, and E. Balish. "B cell-independent selection of memory T cells after mucosal immunization with Candida albicans." Journal of Immunology 158, no. 9 (May 1, 1997): 4328–35. http://dx.doi.org/10.4049/jimmunol.158.9.4328.

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Abstract B cell-deficient mice have normal T cell responses to Ags inoculated systemically; however, it is not known whether they can mount systemic and mucosal T cell responses to Ags through normally B cell-enriched gastrointestinal mucosae. Mucosal colonization of germfree, B cell-deficient J(H)D mice with the pathogenic gastrointestinal fungus, Candida albicans selected splenic CD4+ and CD8+ TCR alphabeta memory T cells, as indicated by 1) increased numbers of splenic CD4+ and CD8+ TCR alphabeta expressing T cells of the CD45RB(low) CD44(high) phenotype, 2) early expansion followed by progressive decrease in the number of splenic CD4+ and CD8+ TCR alphabeta T cells, and 3) concomitant increases in the percentage of apoptosis and proliferation in the latter subsets. Although i.v. challenge of germfree or conventional J(H)D mice with C. albicans did not increase apoptosis or induce changes in the number of splenic memory T cells, i.v. challenge of mucosally immunized germfree J(H)D mice led to further proliferation and expansion of activated splenic CD4+ and CD8+ TCR alphabeta thymic-educated memory T cells, which were first evoked by mucosal immunization. Oral colonization with C. albicans also increased the number of gammadelta and thymic and extrathymic alphabeta T cells in gastrointestinal mucosae. In conclusion, our results are the first strong evidence that thymic and extrathymic T cells participate in mucosal immunity to C. albicans in the absence of B cells; however, CD4+ and thymic-educated CD8+ TCR alphabeta memory subsets evoked by mucosal, but not parenteral (i.v.), challenge contribute to protective immunity to systemic candidiasis.

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Karaulov, A. V., S. S. Afanasiev, A. M. Zatevalov, Yu V. Nesvizhsky, E. A. Voropaeva, M. S. Afanasiev, N. L. Bondarenko, et al. "DISCRIMINANT ANALYSIS IN ESTABLISHING THE RELATIONSHIP OF PATHOGENETIC MECHANISMS OF GESTATIONAL COMPLICATIONS IN UROGENITAL INFECTION IN PREGNANT WOMEN." Russian Clinical Laboratory Diagnostics 65, no. 7 (June 4, 2020): 443–53. http://dx.doi.org/10.18821/0869-2084-2020-65-7-443-453.

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The aim of the work - to establish the interconnection and interdependence of toll-like mediated pathogenetic mechanisms of urogenital infection in pregnant women from the position of epigenomics. Using discriminant analysis in 89 patients with urogenital infection in pregnant women for the first time was established a reliable evidence-based relationship and interdependence between mucosal immunity, the severity of the infectious process, clinical manifestations, symptoms of miscarriage in the background of simultaneous development of the infectious process and pregnancy. For urgent delivery (infection), urgent childbirth (infection and clinical manifestation) and premature birth, mucosal immunity determines the severity of anti-infective resistance (with increasing mucosal immunity oppression of infectious process and clinical manifestations is logged , and its decrease increases the severity of infection process and clinical manifestations); the inhibition of mucosal immunity prevails over its hyperreaction (inhibition of mucosal immunity is determined by the physiological immunodepression in response to the development of pregnancy, as well as in response to herpes virus infection when activated); the severity of the infectious process depends on the severity of clinical manifestations and symptoms of miscarriage. During miscarriage mucosal immunity provides the pathophysiological course of infectious process and the clinical manifestations and development of symptoms of misacrriage; increasing levels of mucosal immunity to hyperreaction contributes to the development of symptoms of abortion and miscarriage; not registered mutual influence of oppression, mucosal immunity and its hyperreaction; the severity of the infectious process does not depend on the severity of clinical signs and symptoms of miscarriage. In urgent childbirth (infection), the oppression of mucosal immunity does not affect the severity of clinical manifestations, symptoms of abortion and the infectious process. In urgent or premature birth, and termination of pregnancy, the oppression of mucosal immunity affects the severity of clinical manifestations, the severity of the infectious process and the symptoms of abortion; the severity of clinical manifestations and the severity of the symptoms of abortion are interrelated. In urgent birth (infection) mucosal immunity overreaction affects the severity of clinical manifestations, symptoms of miscarriage and infection; in case of term and preterm labour overreaction mucosal immunity on the severity of infection and symptoms of abortion and does not affect the severity of clinical manifestations and at the termination of a pregnancy mucosal immunity on the severity of the infectious process and does not affect the severity of clinical signs and symptoms of abortion. The levels of mucosal immunity inhibition, its hyperreaction, clinical manifestations, symptoms of pregnancy termination and the severity of the infectious process do not depend on the type of herpes simplex virus. In the absence of infection with herpes simplex virus in patients with urogenital infections of pregnant women, there is no mutual influence and the relationship between the oppression of mucosal immunity and hyperreaction of mucosal immunity, the oppression of mucosal immunity prevails over its hyperreaction. With increasing mucosal immunity oppression, increased anti-infectious resistance of the body (the decreased activity of the infectious process), and with its decrease decreased (increased activity of the infectious process). Hyperreaction of mucosal immunity influenced the severity of pregnancy termination symptoms, clinical manifestations and infectious process, and also determined the severity of pregnancy termination symptoms. The severity of the infectious process and clinical manifestations influenced the symptoms of abortion. The severity of the infectious process did not affect the clinical manifestations. During infection with herpes simplex virus type I or type I and II on the background prevalence of oppression mucosal immunity over hyperreaction mucosal immunity, the presence of relationships between them, and the impact of mucosal immunity on the severity of the infectious process and the clinical manifestations increase mucosal immunity has been shown to decrease the severity of infection and clinical manifestations (reduction of anti-infective resistance), while reducing mucosal immunity the severity of infection and clinical manifestations increased. Hyperreaction of mucosal immunity influenced the severity of pregnancy termination symptoms and determined the severity of pregnancy termination symptoms. The severity of the infectious process and clinical manifestations influenced the symptoms of abortion. The severity of clinical manifestations reflects the severity of the infectious process. In type I and type II of pregnancy, the level of mucosal immunity determines the anti-infectious resistance of the body in urogenital infection of pregnant women. Inhibition of mucosal immunity and its hyperreactions are interrelated, have an impact on each other, as a result of their integral interaction, increasing the levels of mucosal immunity leads to a decrease in the severity of clinical manifestations and the infectious process, reducing the levels of mucosal immunity contributes to the manifestation of clinical manifestations, as well as increasing the severity of the infectious process. Hyperreaction of mucosal immunity affects the severity of symptoms of abortion, infection and clinical manifestations. The infectious process and clinical manifestations determine the severity of the symptoms of abortion. In type III and type IV of pregnancy course, there is no mutual influence of mucosal immunity oppression and its hyperreaction. The levels of indicators of mucosal immunity oppression and its hyperreaction are interrelated; the increase in the severity of mucosal immunity oppression is accompanied by a decrease in clinical manifestations and severity of the infectious process and vice versa. Hyperreaction of mucosal immunity affects the severity of symptoms of abortion, infection and clinical manifestations. The infectious process determines the severity of the symptoms of abortion and clinical manifestations, acting as a leading component of gestational complications in urogenital infection of pregnant women. In the III type of pregnancy course oppression of mucosal immunity does not affect the severity of symptoms of miscarriage. In the IV type of pregnancy course, the levels of mucosal immunity oppression prevail over the indicators of mucosal immunity hyperreaction, which is due to the integral interaction of physiological inhibition of immunological reactivity of the organism in response to pregnancy and inhibition of immunological reactivity of the organism, accompanying the activation of infectious process of viral genesis. Hyperreaction of mucosal immunity determines the symptoms of abortion.

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Uddin, Taher, Jason B. Harris, Taufiqur Rahman Bhuiyan, Tahmina Shirin, Muhammad Ikhtear Uddin, Ashraful Islam Khan, Fahima Chowdhury, et al. "Mucosal Immunologic Responses in Cholera Patients in Bangladesh." Clinical and Vaccine Immunology 18, no. 3 (January 19, 2011): 506–12. http://dx.doi.org/10.1128/cvi.00481-10.

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ABSTRACTVibrio choleraeO1 causes dehydrating diarrhea with a high mortality rate if untreated. The infection also elicits long-term protective immunity. SinceV. choleraeis noninvasive, mucosal immunity is likely important for protection. In this study, we compared humoral immune responses in the duodenal mucosa and blood of cholera patients at different time points after the onset of disease and compared them with those of healthy controls (HCs). Immune responses to lipopolysaccharide (LPS) and the recombinant cholera toxin B subunit (rCTB) were assessed by enzyme-linked immunosorbent assay (ELISA) and enzyme-linked immunospot (ELISPOT) assay. Significant increases inV. choleraeLPS-specific IgA and IgG antibody levels were seen in duodenal extracts on day 30, but the levels decreased to baseline by day 180; plasmaV. choleraeLPS-specific IgA levels remained elevated longer. Levels of mucosal CTB antibodies also peaked on day 30, but the increase reached statistical significance only for IgG. A significant correlation was found between the CTB antibody-secreting cell (ASC) response in the circulatory system on day 7 and subsequent CTB-specific IgA levels in duodenal extracts on day 30 and the numbers of CTB-specific IgA ASCs in duodenal tissues on day 180. The proportion (0.07%) of mucosalV. choleraeLPS IgA ASCs peaked on day 30 and remained elevated through day 180 compared to that of HCs (P= 0.03). These results suggest that protective immunity againstV. choleraeis not likely mediated by the constitutive secretion of antibodies at the mucosal surface; our results are consistent with those of other studies that suggest instead that anamnestic immune responses of mucosal lymphocytes may play a major role in protection against cholera.

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