Suicide: An Immunological Disorder?

2021 ◽  
Author(s):  
Kalina O'Connor
Keyword(s):  
Immunological Disorder

scholarly journals The enrichment of neutrophil extracellular traps impair the placentas of systemic lupus erythematosus through accumulating decidual NK cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Meng Jiang ◽  
Nan Shen ◽  
Haibo Zhou ◽  
You Wang ◽  
Sihan Lin ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Nk Cells ◽  
Lupus Erythematosus ◽  
Neutrophil Extracellular Traps ◽  
Clinical Samples ◽  
Systemic Lupus ◽  
Extracellular Traps ◽  
Fetal Birth Weight ◽  
Immunological Disorder ◽  
Adverse Pregnancy

AbstractDespite the advances made in the management of pregnancies in women with systemic lupus erythematosus (SLE), the rate of adverse pregnancy outcomes is still higher than that in the general population. In the last few years, neutrophil extracellular traps (NETs) were proven to be detrimental in both autoimmune diseases and placental injury. We investigated whether NETs could be detected in the placentas of pregnant individuals with SLE and explored the relationship between NETs and decidual natural killer cells (dNKs), which comprise the majority of immune cells at the maternal–fetal interface, using clinical samples and animal models. In this study, we found that the infiltration of NETs and dNKs, especially CD56+CD16+ NK cells, was significantly increased in pregnant individuals with SLE with placental insufficiency. In the murine models of SLE, the number of dNKs was significantly decreased due to the decreased formation of NETs affected by Ly6G. Moreover, the histopathological placental injury was reduced, with a remarkable increase in fetal birth weight. This study shows that NETs may contribute to immunological disorder in the placenta and the pathological changes in pregnancies with SLE, which provides a research basis for further explorations of the mechanism of SLE in placental impairment.

scholarly journals Anti-Allergic Potential of Cinnamaldehyde via the Inhibitory Effect of Histidine Decarboxylase (HDC) Producing Klebsiella pneumonia

Molecules ◽  
2020 ◽  
Vol 25 (23) ◽  
pp. 5580
Author(s):  
Lorina I. Badger-Emeka ◽  
Promise Madu Emeka ◽  
Krishnaraj Thirugnanasambantham ◽  
Hairul Islam M. Ibrahim
Keyword(s):  
Mast Cell ◽  
Cell Activation ◽  
Histidine Decarboxylase ◽  
Cell Model ◽  
In Vitro Study ◽  
Inhibitory Effect ◽  
Mast Cell Activation ◽  
Klebsiella Pneumonia ◽  
Immunological Disorder

Allergy is an immunological disorder that develops in response to exposure to an allergen, and histamines mediate these effects via histidine decarboxylase (HDC) activity at the intracellular level. In the present study, we developed a 3D model of Klebsiella pneumoniae histidine decarboxylase (HDC) and analyzed the HDC inhibitory potential of cinnamaldehyde (CA) and subsequent anti-allergic potential using a bacterial and mammalian mast cell model. A computational and in vitro study using K. pneumonia revealed that CA binds to HDC nearby the pyridoxal-5′-phosphate (PLP) binding site and inhibited histamine synthesis in a bacterial model. Further study using a mammalian mast cell model also showed that CA decreased the levels of histamine in the stimulated RBL-2H3 cell line and attenuated the release of β-hexoseaminidase and cell degranulation. In addition, CA treatment also significantly suppressed the levels of pro-inflammatory cytokines TNF-α and IL-6 and the nitric oxide (NO) level in the stimulated mast cells. A gene expression and Western blotting study revealed that CA significantly downregulated the expressions of MAPKp38/ERK and its downstream pro-allergic mediators that are involved in the signaling pathway in mast cell cytokine synthesis. This study further confirms that CA has the potential to attenuate mast cell activation by inhibiting HDC and modifying the process of allergic disorders.

scholarly journals Tools Used to Measure the Physical State of Women with Celiac Disease: A Review with a Systematic Approach

2020 ◽  
Vol 17 (2) ◽  
pp. 539
Author(s):  
Alejandro Martínez-Rodríguez ◽  
Daniela Alejandra Loaiza-Martínez ◽  
Javier Sánchez-Sánchez ◽  
Pablo J. Marcos-Pardo ◽  
Soledad Prats ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Selection Process ◽  
Immunoglobulin A ◽  
Clinical History ◽  
Diagnostic Tools ◽  
Intestinal Biopsy ◽  
Specific Protocol ◽  
Small Intestinal Biopsy ◽  
Immunological Disorder ◽  
Meta Analyses

Celiac disease (CD) is an immunological disorder that mainly affects the small intestine, generating an inflammatory process in response to the presence of gluten (a protein). Autoimmune diseases are part of a group of diseases that are difficult to diagnose without a specific protocol or consensus to detect them due to the number of symptoms and diseases with which it has a relationship. Therefore, the aim of this review was to analyze the diagnostic tools of CD used in middle-aged women, to compare the use and effectiveness of the different tools, and to propose a strategy for the use of the tools based on the results found in the literature. The present research followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guideline. The search was conducted in the following databases: Scielo, PubMed, Web of Science, and Worldwide Science org. In the initial literature search, 2004 titles and relevant abstracts were found. Among them, 687 were duplicates, leaving 1130 articles. Based on the inclusion criteria, only 41 articles passed the selection process; 4 main types of analyses appear in the studies: blood tests, questionnaires, clinical history, and biopsy. It can be said that none of the analyses have a 100% reliability since most of them can present false negatives; therefore, the best way to diagnose celiac disease up to now is through a combination of different tests (Immunoglobulin A and small intestinal biopsy).

scholarly journals Spontaneous (Primary) Candida peritonitis

1995 ◽  
Vol 9 (3) ◽  
pp. 144-146
Author(s):  
Joe Sukhabote ◽  
Hugh J Freeman
Keyword(s):  
Candida Albicans ◽  
Abdominal Pain ◽  
Gastrointestinal Tract ◽  
Amphotericin B ◽  
Ascitic Fluid ◽  
Systemic Candidiasis ◽  
Local Infection ◽  
Immunological Disorder ◽  
Candida Peritonitis

A 49-year-old female presented with abdominal pain and ascites. Subsequent investigations revealedCandida albicansin the ascitic fluid without evidence of systemic candidiasis or a source of local infection in another site. Additional studies revealed no evident underlying immunological disorder and the gastrointestinal tract was intact. Therapy with amphotericin B led to resolution of abdominal pain and ascites with no recurrence.

Immunological disorder and Hirschsprung disease in round femoral inferior epiphysis dysplasia

1995 ◽  
Vol 4 (2) ◽  
pp. 130???135 ◽  
Author(s):  
M. LECORA ◽  
G. PARENTI ◽  
E. IACCARINO ◽  
G. SCARANO ◽  
S. CUCCHIARA ◽  
...  
Keyword(s):  
Hirschsprung Disease ◽  
Immunological Disorder

scholarly journals Very Early Involvement of Innate Immunity in Peripheral Nerve Degeneration in SOD1-G93A Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Daniela Francesca Angelini ◽  
Federica De Angelis ◽  
Valentina Vacca ◽  
Eleonora Piras ◽  
Chiara Parisi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Clinical Evidence ◽  
Nerve Degeneration ◽  
Adaptive Immune ◽  
Neural Damage ◽  
Immunological Disorder ◽  
Sciatic Nerves ◽  
Old Mice ◽  
Circulating Levels ◽  
Lateral Sclerosis

Recent preclinical and clinical evidence suggest that immune system has a role in the progression and prognosis of Amyotrophic Lateral Sclerosis (ALS), but the identification of a clear mechanism and immune players remains to be elucidated. Here, we have investigated, in 30 and 60 days (presymptomatic) and 120 days (symptomatic) old SOD1-G93A mice, systemic, peripheral, and central innate and adaptive immune and inflammatory response, correlating it with the progression of the neurodegeneration in neuromuscular junction, sciatic nerves, and spinal cord. Surprisingly, we found a very initial (45–60 days) presence of IgG in sciatic nerves together with a gradual enhancement of A20/TNFAIP3 (protein controlling NF-κB signalling) and a concomitantly significant increase and activation of circulating mast cells (MCs) as well as MCs and macrophages in sciatic nerve and an enhancement of IL-6 and IL-10. This immunological frame coincided with a myelin aggregation. The 30–60 days old SOD1-G93A mice didn’t show real elements of neuroinflammation and neurodegeneration in spinal cord. In 120 days old mice macrophages and monocytes are widely diffused in sciatic nerves, peripheral neurodegeneration reaches the tip, high circulating levels of TNFα and IL-2 were found and spinal cord exhibits clear signs of neural damage and infiltrating immune cells. Our results underpin a clear immunological disorder at the origin of ALS axonopathy, in which MCs are involved in the initiation and sustaining of inflammatory events. These data cannot be considered a mere epiphenomenon of motor neuron degeneration and reveal new potential selective immune targets in ALS therapy.

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