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).
Local Stress-Limiting Systems and their Cardioprotective Effects
Felix Z. Meerson, Alexander V. Galkin in Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
Hence, PGs can be supposed to prevent stress damages or diseases provoked by the stress reaction. The protective effect of PGs is most definite in stress ulceration of the gastric mucosa. Such lesions produced in rats by a 2-h immobilization stress are efficiently averted with prior administration of PGE.91 Recently, the development of gastric stress ulcers has been found to depend on the endogenous PG level in the gastric mucosa. Ulceration in immobilization92 and other93 types of stress is associated with a decline in PGE2, PGI2, et seq. in the mucosa. Prior activation of PG synthesis by intragastric administration of arachidonic acid prevents both the PGE2 drop and ulceration.92 It has also been shown that the known antiulcerous action of the histamine H2-receptor blocker famotidine is due to the fact that the drug prevents the stress-induced decline in gastric mucosal PG.93 PGs provide protection against such damages by preventing gastric vasoconstriction owing to their vasodilatory properties, and by stabilizing the gastric cell membranes.
Histopathology of the Nasal Cavity in Laboratory Animals Exposed to Cigarette Smoke and Other Irritants
D. V. M. Gerd Reznik, Sherman F. Stinson in Nasal Tumors in Animals and Man, 2017
As the normal entrance to the respiratory tract, the nasal cavity is the first target for airborne irritants and the first physical barrier impeding their progress to the lower conducting airways. It thus has a protective function for which it is well-designed, not only to provide but also to maintain by preserving its own integrity. Primarily, its intricate structure and large surface area encourage the inertial impaction of coarse particles, those with mass median aerodynamic diameter of about 10 μm or more. Secondly, its mucosa rich in goblet and ciliated cells promotes their mucociliary clearance, at the same time humidifying the air. Finally, its extensive vasculature facilitates absorption to reduce pulmonary insult and, if necessary, expedites inflammatory response. If these defensive mechanisms are impaired, the risk of damage to the lower respiratory system increases. It is therefore important, in the experimental evaluation of inhaled irritants, to examine the nasal cavity not only for induced damage but also for preexisting coincidental or spontaneous disease. Also, histo-pathological examination of this region is essential for data on pharmaceutical preparations to be administered by the nasal route.1 Surprisingly, because of its obvious significance, the nasal cavity has been ignored in many inhalation studies. Omissions have been attributed to dearth of anatomical knowledge, technical difficulties, and, paradoxically, to the possibility of infection complicating the results.2,3
Current status and advances in esophageal drug delivery technology: influence of physiological, pathophysiological and pharmaceutical factors
Published in Drug Delivery, 2023
Ai Wei Lim, Nicholas J. Talley, Marjorie M. Walker, Gert Storm, Susan Hua
The average thickness of the esophageal wall is approximately 1.87 to 2.70 mm in the dilated state and 4.05 to 5.68 mm in the contracted state (Xia et al., 2009). The thickness of the esophageal wall has also been reported to be slightly larger in males (5.26 mm) compared to females (4.34 mm) (Xia et al., 2009). The wall of the esophagus is comprised of the mucosa, submucosa, and muscularis propria (Figure 1). In healthy individuals, the mucosa is composed of three layers – non-keratinized, stratified squamous epithelium; lamina propria (composed of connective tissue); and muscularis mucosa (Scott-Brown et al., 2008; Orlando, 2010; Standring, 2020). The muscularis mucosa is composed primarily of smooth muscle, with a combination of striated muscles at the upper part of the esophagus. The submucosa layer consists of predominantly blood vessels, lymphatic vessels, minor salivary glands, connective tissues, and autonomic nerve plexus (i.e. submucosal plexus). The muscularis propria is formed by a mixture of striated and smooth muscles and is responsible for motor functions of the esophagus.
Bacterial imbalance and gut pathologies: Association and contribution of E. coli in inflammatory bowel disease
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Shahanavaj Khan, Ahamad Imran, Abdul Malik, Anis Ahmad Chaudhary, Abdur Rub, Arif Tasleem Jan, Jakeera Begum Syed, Christian Rolfo
The diverse population and activity of the gut microbiota have coevolved along with the host since birth [28]. It is progressively manifest that gut microbes play an important role in shaping the host immune and metabolic pathways and eventually in affecting the health of the host [29,30]. The gut is protected from inhabitant microbes. The exposure of the mucosal tissue of host cell to bacteria is limited by the presence of a layer of mucus secreted by goblet cells in the epithelium, although commensal bacteria-mediated changes in the availability or use of energy substrates may indirectly influence the homeostasis and normal function of immune cells [31–33]. The presence of mucus and their mediators is essential for regulating homeostasis at the mucosal barrier. The lamina propria possesses many immune cells such as macrophages, lymphoid cells, neutrophils, dendritic cells, B cells, and T cells, which are involved in mucosal immunity and homeostasis of the intestine (Figure 1) [34]. The outermost layer of the lamina propria secretes mucus that helps to entrap the bacterial population and prevent their translocation into the tissue.
miRNA and mRNA expression profiling reveals potential biomarkers for metastatic cutaneous melanoma
Published in Expert Review of Anticancer Therapy, 2021
Jun Wang, Yiye Tao, Queqiao Bian
Malignant melanoma originates from the uncontrolled abnormal proliferation of neural crest melanocytes with a sharply increasing morbidity rate worldwide [1]. It is most commonly located in the skin, mucosa, eyes, and gastrointestinal tract. The majority of the patients develop cutaneous melanoma (CM), mainly due to frequent UV light exposure [2]. Epidemiological evidence demonstrates that CM accounts for approximately 5% of all skin cancers and is regarded as one of the most aggressive and lethal skin malignancies [3]. Overcoming this cancer type is challenging, owing to its high metastasis and recurrence. At present, significant advances have been introduced in the treatment of CM, in particular with the revolution of targeted therapy and immunotherapy [4–6]. However, effective and promising therapies are currently unavailable for metastatic CM [7–9]. Early detection and targeted treatment hold a better prognosis for patients with CM metastasis. However, due to the metastasis of melanoma, early detection of CM is still limited. Therefore, it is necessary to find more novel biomarkers for metastatic CM.
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