Role of T lymphocytes in intestinal mucosal injury

Celiac disease is a disorder characterized by a permanent sensitivity to gluten, such that its presence in the diet induces an enteropathy. Exposure of susceptible individuals to gluten-containing foods causes small intestinal mucosal injury associated with malabsorption of variable severity. The association between the occurrence of malabsorption and the presence of wheat or rye in the diet was first recognized by Dicke in 1950. Subsequently, barley was also shown to be toxic. The role of oats in producing disease remains controversial, but rice and maize are known not to cause disease. EPIDEMIOLOGY Celiac disease is one of the most frequent causes of malabsorption during childhood, with prevalence rates of between 1:500 and 1:3000 commonly quoted in the literature. Although the exact prevalence in any particular region is difficult to determine, marked geographical variations do appear to exist. A preyalence rate of 1:300 has been reported in western Ireland. Similarly, celiac disease is reported more frequently in patients from European countries than from North America. There is some evidence that the incidence may also be changing. Based on studies from the United Kingdom, it has been suggested that the incidence of childhood celiac disease may have been declining in recent years, following a peak in the early 1970s.

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Role of melatonin in intestinal mucosal injury induced by restraint stress in mice

Pharmaceutical Biology ◽

10.1080/13880209.2020.1750659 ◽

2020 ◽

Vol 58 (1) ◽

pp. 342-351 ◽

Cited By ~ 1

Author(s):

Rutao Lin ◽

Zixu Wang ◽

Jing Cao ◽

Ting Gao ◽

Yulan Dong ◽

...

Keyword(s):

Restraint Stress ◽

Mucosal Injury ◽

Intestinal Mucosal Injury

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Platelet-activating factor-induced microvascular dysfunction: role of adherent leukocytes

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1990.258.1.g158 ◽

1990 ◽

Vol 258 (1) ◽

pp. G158-G163 ◽

Cited By ~ 8

Author(s):

P. Kubes ◽

M. Suzuki ◽

D. N. Granger

Keyword(s):

Protein Concentration ◽

Ischemia Reperfusion ◽

Platelet Activating Factor ◽

Microvascular Dysfunction ◽

Fold Increase ◽

Mucosal Injury ◽

Plasma Protein Concentration ◽

Intestinal Mucosal Injury ◽

Adherent Leukocytes

Platelet-activating factor (PAF) has been implicated in the pathogenesis of intestinal mucosal injury associated with endotoxemia, inflammation, allergic reactions, and ischemia-reperfusion. Although it is generally held that PAF initiates mucosal injury by enhancing transcapillary fluid and protein exchange, the effects of PAF on the intestinal microvasculature have not been defined to date. In this study we examined the influence of local intrarterial infusions of PAF (4, 20, and 40 ng/min) on intestinal transcapillary, lymphatic, and transmucosal water and protein fluxes. All of these parameters were increased by each of the concentrations of PAF. PAF caused a large rise in venous hematocrit without a corresponding increase in venous plasma protein concentration and a 14- to 37-fold increase in vascular protein flux. Local intra-arterial infusion of PAF promoted leukocyte adherence to mesenteric venular endothelium, a process that is inhibited by the monoclonal antibody, MoAb IB4. PAF-induced increments in intestinal lymph flow, venous hematocrit, and vascular protein flux were greatly attenuated in animals treated with MoAb IB4. The results of this study indicate that PAF promotes the filtration of fluid and protein across intestinal capillaries. These microvascular effects of PAF are mediated, in part, by adherent leukocytes.

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Role of neutrophils in intestinal mucosal injury

Journal of the American Veterinary Medical Association ◽

10.2460/javma.2000.217.498 ◽

2000 ◽

Vol 217 (4) ◽

pp. 498-500 ◽

Cited By ~ 13

Author(s):

J'mai M. Gayle ◽

Anthony T. Blikslager ◽

Samuel L. Jones

Keyword(s):

Mucosal Injury ◽

Intestinal Mucosal Injury

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PD-L1 Inhibitors for the Treatment of Prostate Cancer

Current Drug Targets ◽

10.2174/1389450121666200609142219 ◽

2020 ◽

Vol 21 (15) ◽

pp. 1558-1565

Author(s):

Matteo Santoni ◽

Francesco Massari ◽

Liang Cheng ◽

Alessia Cimadamore ◽

Marina Scarpelli ◽

...

Keyword(s):

Prostate Cancer ◽

Clinical Trials ◽

T Lymphocytes ◽

Chronic Inflammation ◽

Immune Cells ◽

Response To Therapy ◽

Complex Series

The carcinogenesis of prostate cancer (PCa) results from a complex series of events. Chronic inflammation and infections are crucial in this context. Infiltrating M2 type macrophages, as well as neutrophils and T lymphocytes, contribute to PCa development, progression and response to therapy. The preliminary findings on the efficacy of immunotherapy in patients with PCa were not encouraging. However, a series of studies investigating anti-PD-L1 agents such as Atezolizumab, Avelumab and Durvalumab used alone or in combination with other immunotherapies, chemotherapy or locoregional approaches are in course in this tumor. In this review, we illustrate the role of immune cells and PD-L1 expression during PCa carcinogenesis and progression, with a focus on ongoing clinical trials on anti-PD-L1 agents in this context.

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Mitochondria, Oxidative Stress, cAMP Signalling and Apoptosis: A Crossroads in Lymphocytes of Multiple Sclerosis, a Possible Role of Nutraceutics

Antioxidants ◽

10.3390/antiox10010021 ◽

2020 ◽

Vol 10 (1) ◽

pp. 21

Author(s):

Anna Signorile ◽

Anna Ferretta ◽

Maddalena Ruggieri ◽

Damiano Paolicelli ◽

Paolo Lattanzio ◽

...

Keyword(s):

Oxidative Stress ◽

Multiple Sclerosis ◽

T Lymphocytes ◽

Main Role ◽

Apoptosis Resistance ◽

Nutraceutical Compounds ◽

Camp Pathway ◽

Central Nervous Systems ◽

Genetic And Environmental Factors

Multiple sclerosis (MS) is a complex inflammatory and neurodegenerative chronic disease that involves the immune and central nervous systems (CNS). The pathogenesis involves the loss of blood–brain barrier integrity, resulting in the invasion of lymphocytes into the CNS with consequent tissue damage. The MS etiology is probably a combination of immunological, genetic, and environmental factors. It has been proposed that T lymphocytes have a main role in the onset and propagation of MS, leading to the inflammation of white matter and myelin sheath destruction. Cyclic AMP (cAMP), mitochondrial dysfunction, and oxidative stress exert a role in the alteration of T lymphocytes homeostasis and are involved in the apoptosis resistance of immune cells with the consequent development of autoimmune diseases. The defective apoptosis of autoreactive lymphocytes in patients with MS, allows these cells to perpetuate, within the CNS, a continuous cycle of inflammation. In this review, we discuss the involvement in MS of cAMP pathway, mitochondria, reactive oxygen species (ROS), apoptosis, and their interaction in the alteration of T lymphocytes homeostasis. In addition, we discuss a series of nutraceutical compounds that could influence these aspects.

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