Host–Biofilm Interactions at Mucosal Surfaces and Implications in Human Health
Chaminda Jayampath Seneviratne in Microbial Biofilms, 2017
Mucosae are moist linings of the gastrointestinal, nasal and other orifices of the body in continuum with the skin at body openings. The term mucosa signifies a protective mucous membrane at these sites. The mucus thus secreted serves to prevent the invasion of the body by pathogenic microorganisms. In the past, therefore, host–microbial interactions at the mucosal surfaces were studied based on the notion that microorganisms exhibited a free-floating or ‘planktonic’ mode of growth. Hence, the precept of a ‘mucosal biofilm’ on mucosal surfaces remained unrecognised until recently. The advent of technology such as DNA sequencing has unravelled that even under healthy conditions, mucosal surfaces house a resident microbiota or mucosal microbiome comprising diverse bacteria and fungi [2]. It is therefore interesting to examine the circumstance under which the mucosal microbial community will develop into a pathogenic biofilm due to a disruption of the microbial balance (termed dysbiosis), compromised host defences or an invasion by a non-resident pathogenic organism capable of overcoming the host immune defences. Mucosal biofilm–associated infections can lead to serious health consequences and are linked with various human diseases including obesity and inflammatory bowel disease (IBD).
Secreted effectors of the innate mucosal barrier
Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald in Principles of Mucosal Immunology, 2020
The mucosal surfaces, including the surface of the eye and the linings of the gastrointestinal, respiratory, reproductive, and urinary tracts, are the major interface between mammalian tissues and the potentially hostile external environment. Mucosal surfaces have evolved a well-regulated barrier to protect against chemical, physical, and microbial insults. In the intestinal tract, this barrier consists of epithelial cells, a secreted layer of mucus produced by goblet cells, and antimicrobial peptides released by the gastric and colonic epithelium and by small intestinal Paneth cells (Figure 4.1). In this chapter, we describe the components of this barrier and their regulation by innate and adaptive immunity, focusing mainly on the intestinal tract because it is the most thoroughly studied mucosal tissue and is continuously exposed to potential infection.
Hormones as Immune Modulating Agents
Thomas F. Kresina in Immune Modulating Agents, 2020
Mucosal surfaces are constantly bombarded with antigen, infectious agents, irritants, and toxins, many of which have the capacity to stimulate the immune system and/or to elicit inflammation. An exaggerated mucosal response to a mild irritant (e.g., asthma) is just as dangerous as an inadequate response to a pathogenic agent. Therefore, the immune/inflammatory response must be strictly controlled on mucosal surfaces at a level which assures adequate responses against pathogenic agents and detoxification and clearance of harmful agents by inflammatory cells, yet the inflammatory response must not be excessive. Because mucosal surfaces fall outside the body, the capacity of the immune system to distinguish self from nonself is virtually useless in this situation. We suggested earlier that immunoregulatory substances produced by salivary glands, especially in the submandibular gland in laboratory rodents, are fundamental to immunoregulation in the gastrointestinal tract. Of these substances, nerve growth factor, transforming growth factor-β, epidermal growth factor, and glandular kallikrien are most important. The sympathetic nervous system regulates the secretion of these substances. Through this neuroimmunoregulatory function the submandibular gland is suggested to play a key role in the regulation of mucosal immune and inflammatory responses [396]. This hypothesis is supported by clinical observations that the failure of the major salivary glands (Sjogren disease) in humans is frequently associated with rheumatoid diseases, indicating a systemic disturbance of immunoregulation [396].
Recent advances on biodegradable polymeric carrier-based mucosal immunization: an overview
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Lovedeep Kaur, Ankush Sharma, Awesh Kumar Yadav, Neeraj Mishra
This mucosal-associated lymphoid tissue (MALT) lies along the mucosa of the respiratory, gastrointestinal, and genitourinary tracts as totals as bronchus-related lymphoid tissue (BALT), gut-associated lymphoid tissue (GALT) and nasal-associated lymphoid tissue (NALT) [4]. The GALT is represented by the Peyer’s patches (PP), the appendix and small solitary lymphoid nodules connected with microfold (M) cells, antigen-exhibiting cells, microphages and dendritic cells; CD4+ and CD8+ T cells and B cells. These are the effector organs, which evoke mucosal insusceptible reaction. The major characteristic of mucosal immunity is to deliver local insusceptible respond as sIgA which check the contamination of epithelial host [5]. Mucosal surfaces are grouped into two sorts in view of their distinct attributes. Sort I mucosal surfaces are found in the gut alimentary, respiratory and female upper reproductive system, whereas sort II mucosal surfaces are found in the visual, mouth alimentary and female lower reproductive system. Sort I mucosal surfaces have a basic columnar epithelial layer in which IgA is the real immunoglobulin (Ig) isotype. Interestingly, sort II mucosal surfaces have a stratified squamous epithelial layer, and the real Ig isotype is IgG [6] (Table 1).
Preliminary Report on Interleukin-22, GM-CSF, and IL-17F in the Pathogenesis of Acute Anterior Uveitis
Published in Ocular Immunology and Inflammation, 2021
Jerry Chien-Chieh Huang, Matthew Schleisman, Dongseok Choi, Claire Mitchell, Lindsey Watson, Mark Asquith, James T. Rosenbaum
Fourth, this is the first study to our knowledge that has investigated MAIT-like cells or ILC-3 cells, two important populations of innate lymphoid cells, in acute anterior uveitis. We refer to the cells that we have studied as MAIT-like because they express the T cell receptor, V alpha 7.2 as is typical of MAIT cells. We recognize, however, that some conventional T cells might also express this receptor and thus we cannot say definitively that they are MAIT cells. The data do show, however, that cells expressing this receptor and deriving from subjects with AAU expressed an increased frequency of IL-17A, IL-17F, and GM-CSF after stimulation. MAIT cells have a number of interesting features. They are found predominantly at mucosal surfaces.32 They have a very limited T cell receptor repertoire.32 They appear to respond to derivatives of vitamin B.32 We and others have implicated the intestinal microbiome in the pathogenesis of AAU.33 An increase in circulating MAIT cells could be due to activation in the intestine.
Immunoglobulin A antibodies to oxidized collagen type II as a potential biomarker for the stratification of spondyloarthritis from rheumatoid arthritis
Published in Scandinavian Journal of Rheumatology, 2020
C Vinci, M Infantino, S Raturi, A Tindell, LM Topping, R Strollo, H Amital, Y Shoenfeld, S Gertel, V Grossi, M Manfredi, IM Rutigliano, F Bandinelli, F Li Gobbi, A Damiani, P Pozzilli, IB Mcinnes, CS Goodyear, M Benucci, A Nissim
Although the aetiology of SpA remains obscure, it has demonstrated a strong association with environmental factors, including pathogenic intestinal microbes (48). Mucosal surfaces serve as a protective barrier against most pathogens. These surfaces are protected by a first-line defence mediated by IgA (49). Moreover, it is also known that T-helper TH17 cells are more abundantly present on the mucosal surface of the intestine, compared with other T-cell subsets (50). Accumulating evidence has demonstrated that TH17 cells contribute to intestinal homoeostasis by regulating intestinal IgA secretion, supporting a link between intestinal T-cell function and IgA production. Less is known about the potential role of TH17 cells for IgA induction in the joints, although chronic activation of TH17 was shown to induce hyperactive IgA synthesis in many types of inflammatory joint disease. Surprisingly, in the current study we did not observe a significant difference in IgG versus IgA anti-oxPTM-CII reactivity in patients who had IBD associated with axSpA. Thus, the involvement of IgA anti-oxPTM-CII may be a more complex mechanism and further studies of TH17 and IL-17 levels in the various groups may shed light on these mechanisms.
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