Myeloid cells, especially mononuclear phagocytes, which include monocytes, macrophages and dendritic cells (DC), play vital roles in innate immunity, and in the initiation and maintenance of adaptive immunity. While T cell-associated activation pathways and cytokines have been identified and evaluated in inflammatory bowel disease (IBD) patients, the role of mononuclear phagocytes are less understood.

We performed in silico analysis and evaluated the enrichment of immune cells, with a focus on mononuclear phagocytes in IBD patient colonic biopsies. Samples were from different gut locations, with different levels of disease severity, and with treatment response to current therapies. We observe enrichment of monocytes, M1 macrophages, activated DCs and plasmacytoid DCs in inflamed tissues from various gut locations. This enrichment correlates with disease severity. Additionally, the same mononuclear phagocytes subsets are among the top enriched cell types in both infliximab and vedolizumab treatment non-responder samples. We further investigated the enrichment of selected DC and monocyte subsets based on gene signatures derived from a DC- and monocyte-focused scRNA-seq study; and verified enrichment in both inflamed tissues and those with treatment resistance. Moreover, we validated an increased mononuclear phagocyte subset abundance in a Dextran Sulphate Sodium induced colitis model in C57Bl/6 mice representative of chronic inflammation.

We conducted an extensive analysis of immune cell populations in IBD patient colonic samples and identified enriched subsets of monocytes, macrophages and dendritic cells in inflamed tissues.  Understanding how they interact with other immune cells and other cells in the colonic microenvironment such as epithelial and stromal cells will help us to delineate disease pathogenesis.

All treatments for fever are based on the belief  that  fits is the result of  41 degree Celsius temperature and  it  damages cells of  brain and body. At the same time there is no evidence based   tests or concrete  diagnosing  methods  to the  belief  that  fits and brain damage  is the result of  pyrexia [1].

Necessary ingredients to destroy brain cells  and fits cannot be seen  in fever.In pyrexia or absence of fever  a fainted  patient fell on the floor with unconscious state and destroy cells of brain, and necessary ingredients to  become conscious are same.

When disease increases essential blood circulation and energy level also decreases. The vertical height between heart and brain is more than one feet. When the disease becomes severe, ability to pump the  blood to the brain decreases. As a result of this   brain cells are damaged. so the patient might be paralyzed or may even die.

In pyrexia or absence of fever,  when blood flow to the brain decreases and fits are formed. There is no other  way than  this  to increase  blood circulation  to the brain.It is  a sensible and discreet  action of brain to protect the  life or organ.

 Recovery from  Fits.

The patient become conscious before the time to get decreasing the temperature of fever. When the fainted patient lie on the floor, the vertical height between heart and brain is decreased, blood circulation increased to brain.

 Self checking  methods.

When the fainted patient lie on the floor,The patient can stand straight and lie on bed alternatively.Then the patient can experience  himself the intensity of blood circulation.T he patient can experience when he stand  his blood circulation decreases and when lie on the bed the blood circulation decreases.Besides that he can also experience increased blood circulation when lie on the bed raise the foot higher than head.

Inflammation is believed to be a contributing factor in many chronic diseases. The influence of vitamin D deficiency on inflammation is being explored but studies have not demonstrated a causative effect. Low serum 25(OH)D is also found in healthy persons exposed to adequate sunlight. Despite increased vitamin D supplementation inflammatory diseases are increasing. The current method of determining vitamin D status may be at fault. The level of 25(OH)D does not always reflect the level of 1,25(OH)2D. Assessment of both metabolites often reveals elevated 1,25(OH)2D, indicating abnormal vitamin D endocrine function. Some authorities now believe that low 25(OH)D is a consequence of chronic inflammation rather than the cause. Research points to a bacterial etiology pathogenesis for an inflammatory disease process which results in high 1,25(OH)2D and low 25(OH)D. Immunotherapy, directed at eradicating persistent intracellular pathogens, corrects dysregulated vitamin D metabolism and resolves inflammatory symptoms. This article reviews vitamin D’s influence on the immune system, examines the myths regarding vitamin D photosynthesis, discusses ways to accurately assess vitamin D status, describes the risks of supplementation, explains the effect of persistent infection on vitamin D metabolism and presents a novel immunotherapy which provides evidence of an infection connection to inflammation.

NADPH Oxidase (NOX) activity has been suggested to be implicated in a plethora of cellular functions contributing to physiological and pathological conditions. Precise determination of NOX activity is not trivial. Several studies have addressed NOX activity in relation to polymorphisms in cis-acting genetic elements, however, providing much conflicting results. To date, no genetic polymorphism pertinent to one of the NOX subunits has been established as biomarker for NOX activity. We set up to determine activity of the phagocytic NOX by a particular sensitive assay in Lymphoblastoid Cell Lines (LCLs) allowing iterative measurements on the same genetic background. A set of 290 LCLs of Caucasian origin with available genotypic data was split into training and test set by a 2:1 ratio. NOX activity determination was performed initially four times in each LCL at different days each with four same LCLs serving as reference for inter-day comparisons. Stringent criteria to identify outliers of the measurement series were applied to obtain a robust value of the NOX activity for each LCL. If these criteria were not met with at least three independent measurements two to four additional repetitions were conducted. If again applied stringent criteria fail, robustness of repetitive NOX activity measurements, the respective LCL was excluded from further analyses. Measurement series of LCLs which matched the consistency criteria elicited a mean variation coefficient of 17.0% (SD±10.6%). An almost identical distribution of the determined NOX activity was noted for the training and the test set of LCLs. These data prove our method suitable for reliable assessment of NOX activity providing a reliable basis for pending association testing with genotypes. As with 290 LCLs a total of 1500 NOX activity measurements, each time assayed in quadruplicates, were performed, this study is the largest conducted in this context so far.

Background.There are increasing evidences that favor the prenatal beginning of schizophrenia. These evidences point toward intra-uterine environmental factors that act specifically during the second pregnancy trimester producing a direct damage of the brain of the fetus. The current available technology doesn't allow observing what is happening at cellular level since the human brain is not exposed to a direct analysis in that stage of the life in subjects at high risk of developing schizophrenia. Methods. In 1977 we began a direct electron microscopic research of the brain of fetuses at high risk from schizophrenic mothers in order to finding differences at cellular level in relation to controls. Results. In these studies we have observed within the nuclei of neurons the presence of complete and incomplete viral particles that reacted in positive form with antibodies to herpes simplex hominis type I [HSV1] virus, and mitochondria alterations. Conclusion. The importance of these findings can have practical applications in the prevention of the illness keeping in mind its direct relation to the aetiology and physiopathology of schizophrenia. A study of amniotic fluid cells in women at risk of having a schizophrenic offspring is considered. Of being observed the same alterations that those observed previously in the cells of the brain of the studied foetuses, it would intend to these women in risk of having a schizophrenia descendant, previous information of the results, the voluntary medical interruption of the pregnancy or an early anti HSV1 viral treatment as preventive measure of the later development of the illness.

Autoimmune hepatitis is a rare disease of low prevalence that is associated with diagnostic autoantibodies. These autoantibodies are useful disease markers that facilitate the early diagnosis of autoimmune hepatitis for therapeutic intervention to prevent progression to liver cirrhosis and associated complications. Adult onset type-1 autoimmune hepatitis is associated with F-actin reactive smooth muscle SMA-T or SMA-G autoantibody, antinuclear autoantibody in 60% of patients and autoantibody to SLA/LP in 15-20%. Juvenile onset type-2 autoimmune hepatitis is associated with LKM-1 and LC-1 autoantibodies. Liver autoantibodies in asymptomatic patients with normal liver function may precede the subsequent development of overt autoimmune liver disease. For routine diagnostic immunology laboratories, initial screening for smooth muscle SMA-T antibody by immunofluorescence remains the method of choice with confirmation for reactivity with F-actin by immunofluorescence.

Chronic Viral Hepatitis B (VHB) is characterized by a progressive destruction of hepatocytes and T-lymphocyte depletion. The mechanisms of the CD95-CD95L signaling pathway during chronic VHB and cirrhotic process remains unclear. Our objective was to evaluate the involvement of the CD95-CD95L receptor-ligands in T-lymphocyte depletion and hepatic cytolysis in patients with chronic VHB. A cross-sectional study was conducted from September to December 2018, at the Yaoundé General Hospital, Cameroon. Four milliliters of blood were collected and analyzed. The CD95, CD95L levels and CD4+, CD8+ T-cell counts were performed by ELISA and Flow cytometry, respectively. The data were analyzed using EpiInfo 7.0 and GraphPad PRISM 5.0, with the significant threshold set at p ≤ 0.05 and a 95% confidence interval. Of the 130 patients, 36 (27.7%) were cirrhotic, and 94 (72.3%) were non-cirrhotic. The plasma level of CD95 and CD95L were significaly elevated in cirrhotic patients, compared with non-cirrhotic patients (p < 0.001 and p = 0.001 respectively). CD4/CD8 ratios were lower in cirrhotic patients, compared with non-cirrhotic patients (p < 0.001). There were statistically significant correlations between CD95 and CD4+, between CD95 and CD8+, between CD95 and CD4/CD8 ratio, between CD95 and fibrosis scores and between CD95L and fibrosis score. CD95-CD95L could be involved in T-lymphocyte depletion and hepatic cytolysis during the pathogenesis of chronic VHB, and could be used as biomarkers for immunological and hepatic monitoring in patients with chronic VHB.

As you aware, if temperature increases (Absence of  fever)after 31 degree Celsius , Warm sensitive neurons increase their firing rate and inhibit Cold sensitive neurons as core temperature increases. As temperature drops, the firing rate of Warm sensitive neurons decreases, reducing their inhibition, and Cold sensitive neurons which respond by increasing their firing rates.

On the contrary to increase of temperature, in fever the firing rate of Warm sensitive neurons decreases, the firing rate of Cold sensitive neurons increases as core temperature increases. inhibit warm sensitive neurons. The temperature increasing and decreasing controlled by the brain. The firing rate of Warm sensitive neurons and Cold sensitive neurons also controlled by the brain.         

When the disease becomes threat to life or organs, blood circulation decreases. Temperature of fever will emerges to increase prevailing essential blood circulation.

WBC and their products stimulate the brain to increase temperature by increasing the firing rate of Cold sensitive neurons and decreasing the firing rate of Warm sensitive neurons. And it acts as a protective covering of the body to sustain life.There is no  way other than this for a sensible and discreet  brain to increase temperature.

If the aim of   Cold sensitive neurons increasing their firing rates in hypothermia is to increase temperature, then the aim of Cold sensitive neurons  increasing their firing rates during fever is also to increase temperature.

How can we prove that W neurons decreases and C neurons increases in fever to protect the  life or organ?

If we ask any type of question related to fever by assuming that the Warm sensitive neurons decreases and Cold  neurons increases in fever to protect the  life or organ we will get a clear answer. If avoid or evade from this definition we will never get proper answer to even a single question

If we do any type of treatment  by assuming  that the Warm sensitive neurons decreases and Cold  neurons increases in fever to protect the  life or organ , the body will accept, at the same time body will resist whatever treatment to decrease temperature and blood circulation.

No further evidence is required to prove The Warm sensitive neurons decreases and Cold  neurons increases in fever to protect the  life or organ.

Probiotics are live microorganisms, which administered in adequate amounts confer a health benefit on the host. Modulation of the immune response seems to be the common mechanism associated to the consumption of probiotics. Presumably, probiotics must establish a close relationship with Dendritic Cells (DCs), which are able to recognize microbial products by extending their dendrites to the intestinal lumen. Recent studies have shown that DCs activity can be modified following administration of probiotics, especially of the genera Lactobacillus and Bifidobacterium using in vitro methodology. In this sense, the analysis of the host-probiotic interaction represents a dynamic and complex process, which can be studied through tools based on the "omic" sciences. The aim of the present study is to analyze the expression of differential proteins of the interaction between probiotics isolated from breast milk and DCs using proteomics techniques, whereby DCs were generated from peripheral blood monocytes from four healthy participants and were co-cultured with probiotics of the genera Lactobacillus and Bifidobacterium previously isolated from breast milk. After 3 hours of co-cultivation under optimum conditions, the proteins were extracted from each culture, thus generating 2D proteomic maps (SDS-PAGE) and a differential proteomic expression was found derived from the interaction of the co-cultures compared to single cultures. To the moment, our results suggest that the activity of DCs can be successfully regulated by interaction with probiotics.

Background & Aim: Bronchial asthma is an inflammatory airway disease characterized by infiltration of inflammatory cells into bronchial tree and increased airway hyperreactivity to various physical and chemical stimuli. T-cells play an important role in pathogenesis and inflammatory immune response in bronchial asthma. The aim of this study was to detect soluble Interleukin-2 receptors (sIL-2) serum levels, as marker of T lymphocyte activation in vivo, among bronchial asthmatic children. Methods: The study was done at King Abdulaziz University Hospital from January 2015 to December 2015. 77 children were included and subdivided into three groups (acute asthmatic; chronic stable asthmatic and control (table 1, demographic data). After history and clinical examination, with acute asthma were classified into atopic and non-atopic groups. Blood sample was taken from all groups and sIL-2R was measured by ELISA technique. Results: sIL-2R serum level was significantly elevated in acute and chronic asthmatic children versus controls (table 1). Meanwhile, in acute asthmatic, insignificant differences were recorded between different atopic states of the disease (table 2). . Conclusion: This study emphasize the role of T cells in asthma and suggest that regulation of their function may be important in the treatment of acute and stable asthmatic children as evident by elevated serum levels of sIL-2R