user biomichael825's Blog -  - 
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Fri, Aug 3rd - 1:02AM
New solution to response mechanism of the Gram-negative bacteria-induced inflammatory
In July 20,2012, Cell magazine online reported that Gram-negative bacteria infection of the body induce inflammatory response by activating the NLRP3 inflammation through the TRIF signaling pathway.
Being able to induce sepsis syndrome, a systemic inflammatory response beyond control , Gram-negative bacteria is known to lead to high mortality by systemic infection. All along, the molecular mechanisms of the inflammatory reaction occurred in the process of gram-negative bacteremia remains unclear.
This study revealed a TRIF (an inducted¦Â-interferon adapter containing the TIR domain ,and a kind of Toll-like receptor adapter in response to activation ) signaling pathway. All Gram-negative bacteria activate NLRP3 inflammation body through this route (NLRP3 is a member of the Nod-like receptor subfamily in PRR family , can interacte with the adapter protein after activated and activate cysteine proteases -1 (caspase-1
) to form a protein complex inflammatory body ").
Gram-negative bacteria activate caspase-11 through TRIF. And TRIF activate caspase-11 through IF-I signal ,which is necessary and sufficient conditions of induction self-activation of caspase-11. Caspase-11 subsequently synergy regulate caspase-1 activation with assembled NLRP3 inflammation body, and lead to caspase-1-independ cell death. These events particularly occurs in the case with existence of Gram-negative bacteria rather than gram-positive bacteria infection.
The regulatory effect of caspase-11 on TRIF significantly indicates that ,in gram-negative bacterial infection, the Toll-like receptors play an important role as a regulator of inflammation in the body.
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Fri, Aug 3rd - 12:28AM
Regulation and affect of PRL on immune cells
In1989, Hartmann and others studied the affect of exogenous PRL on lymphocyte proliferation in vitro,which have shown that when culturing lymphocytes with PRL antibodies, the transition from G1 phase to S phase of these cells was significantly inhibited. This inhibition can be discharged by adding purified PRL but not GH, indicating that PRL is specific. Mukherjee¡¯s and other studies showed that PRL induced surface IL-2 receptor expression in lymphocyte ,while Other studies showed that PRL plays a necessary role of lymphocyte growth factor in a series of IL-2 initiated reactions. PRL processed macrophages in vitro can increase nitric oxide (NO) and IL-1. PRL can stimulate IFN-gamma and promote the effect of IL-2 in lymphocytes. Considerable evidence suggests that PRL has both acute and chronic effect on the immune response and autoimmunity: PRL activates the protein kinase K have a common effect on T cell proliferation and IL-2. PRL induced IL-2 receptor expression stimulate the generation of IFN-gamma through interferon regulatory factor (IRF-a transcription factor genes) . IRF-1 is an important regulatory factor for differentiation and maturation of T cell and B cell. Thus,PRL stimulating antibody production is related to the increase of the percentage of total lymphocytes and CD2 lymphocytes.
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Fri, Aug 3rd - 12:05AM
Prolactin , autoimmune and autoimmune diseases
The prolactin (PRL) is a multifunctional hormone synthetized by the anterior pituitary and other multiple extrapituitary ingredients including immune cells. Moreover, PRL has a broad impact,on the proliferation and differentiation of a variety of cells in the immune system ,so it is actually a kind of cytokine. PRL receptor (PRL-R) are distributed throughout the immune system, and is a member in cytokine receptor superfamily. There are a series of signaling molecules, among which JAK2, Stat1 and Stat5 has been studied ,involved PRL-R signal transduction.In PRL-activated T cells, PRL can modulate the immune response through the functions of transcription factor genes and interferon regulatory factor-1. The human PRL gene is located near the the major histocompatibility complex (MHC) in short arm of chromosome 6. The human PRL gene polymorphism indicates the PRL generation in lymphocytic cells of SLE. Mild and moderate hyperprolactinemia (HPRL) has been confirmed to exist in 20% -30% of SLE patients, and is related to other initiative disease.. HPRL may play a role in central nervous system lesions of patients lupus nephritis and SLE with. HPRL stimulate the body to produce its own antibodies. The evidence suggests that PRL play an important role in autoimmunity and autoimmune diseases, especially in SLE.
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| August 2012 |
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