Quantitative Biology

1204 Submissions

[2] viXra:1204.0090 [pdf] replaced on 2012-05-10 03:03:16

Acute Respiratory Distress Syndrome is a TH17-Like and Treg Immune Disease

Authors: Wan-Jiung Hu
Comments: 44 Pages.

Acute Respiratory Distress Syndrome (ARDS) is a very severe syndrome leading to respiratory failure and subsequent mortality. Sepsis is the leading cause of acute respiratory distress syndrome. Thus, extracellular bacteria play an important role in the pathophysiology of ARDS. Overactivated neutrophils are the major effector cells in ARDS. Thus, extracellular bacteria triggered TH17-like innate immunity with neutrophil activation counts for the etiology of ARDS. Here, I use microarray analysis to describe TH17-like innate immunity related cytokine including TGF-β and IL-6 up-regulation in whole blood of ARDS patients. Innate TH17 related TLR1,2,4,5,8, HSP70, G-CSF, GM-CSF, complements, defensin, PMN chemokines, cathepsins, Fc receptors, NCFs, FOS, JunB, CEBPs, NFkB, and leukotriene B4 are all up-regulated. TGF-β secreting Treg cells play important roles in lung fibrosis. Up-regulation of Treg associated STAT5B and TGF-β with down-regulation of MHC genes, TCR genes, and costimulation molecule CD86 are noted. Key TH17 transcription factors, STAT3 and RORα, are down-regulated. Thus, the full adaptive TH17 helper CD4 T cells may not be successfully triggered. Many fibrosis promoting genes are also up-regulated including MMP8, MMP9, FGF13, TIMP1, TIMP2, PLOD1, P4HB, P4HA1, PDGFC, HMMR, HS2ST1, CHSY1, and CSGALNACT. Failure to induce successful adaptive immunity could also attribute to ARDS pathogenesis. Thus, ARDS is actually a TH17-like and Treg immune disorder.
Category: Quantitative Biology

[1] viXra:1204.0070 [pdf] submitted on 2012-04-16 20:55:43

Schizophrenia is a TH2 Dominant Autoimmune Disease Possibly Against Acetylcholine Receptors of CNS

Authors: Wan-Jiung Hu
Comments: 19 Pages.

Schizophrenia is a very common psychiatric disorder. However, its etiology and pathogenesis is still unknown. Current theory saying that neurotransmitter imbalance such as serotonin or dopamine only provides limited effectiveness in schizophrenia treatment by drugs changing serotonin and dopamine concentration. Despite of such treatment, majority of schizophrenia patients still have very poor prognosis. Thus, the neurotransmitter imbalance theory is not correct. Here, I propose that schizophrenia is actually a TH2 dominant autoimmune disorder. The candidate of autoantigen could be acetylcholine receptors of CNS. My theory can explain the positive as well as negative symptoms of schizophrenia. By microarray analysis of PBMCS, one-tenth of the total 519 significantly expressed genes are immune-related genes. Among them, TH2 related genes are significantly up-regulated including IL-4, histidine decarboxylase, aldehyde dehydrogenase, CCR9, IgE Fc receptor, GATA2, serotonin receptor, phospholipase A2, and prostaglandin D2 synthase. Besides, TH1 and TH17 related genes are down-regulated including CXCL5, cathepsin C, and neutrophil related S100 binding proteins. The new theory sheds a light to better control this detrimental illness. Anti-inflammatory agents could be used to manage schizophrenia in the near future.
Category: Quantitative Biology