The Prostatitis Foundation

Lipopolysaccharide and interleukin production

 

We have often discussed the possibility that normal urethral flora (Gram-positive bacteria) can release extracellular products which modulate the local immune response (cytokine levels) and therefore predispose to quick or prolonged resolution of symptoms. Here's an interesting study which might shed light on how gut bacteria (whether in the urethra or prostate) or just normal gut bacteria in the gut, releasing a normal product they contain, called lipopolysaccharide (LPS) can influence IL-6 secretion by the pituitary and maybe give rise to some of the symptoms of CPPS and/or chronic fatigue syndrome (CFS).
Dr. Jordan Dimitrakov
Endocrinology 2000 Dec;141(12):4457-65

Lipopolysaccharide directly stimulates the intrapituitary interleukin-6 production by folliculostellate cells via specific receptors and the p38alpha mitogen-activated protein kinase/nuclear factor-kappaB pathway.

Lohrer P, Gloddek J, Nagashima AC, Korali Z, Hopfner U, Pereda MP, Arzt E, Stalla GK, Renner U
Max Planck Institute of Psychiatry, Department of Endocrinology, Munich, Germany.
Bacterial lipopolysaccharide (LPS) activates the immune system and induces increases in peripheral cytokines, which, in turn, affect the endocrine system. In particular, LPS-induced cytokines stimulate the hypothalamic-pituitary-adrenal axis to increase levels of antiinflammatory-acting glucocorticoids.
In the present work, we show that LPS directly stimulates interleukin (IL)-6 release by mouse pituitary folliculostellate (FS) TtT/GF tumor cells and FS cells of mouse pituitary cell cultures.
The stimulatory effect of LPS was strongly enhanced in the presence of serum, suggesting that LPS is only fully active as a complex with LPS-binding protein (LBP). Both TtT/GF cells and mouse pituitaries expressed CD14, which binds the LPS/LBP complex, and Toll-like receptor type 4, which induces LPS signals. LPS increased phospoinositol turnover in TtT/GF cells and induced phosphorylation of p38alpha mitogen-activated protein kinase and the inhibitor (IkappaB) of nuclear factor-kappa B.
Nuclear factor-kappa B was activated by LPS in TtT/GF cells. Functional studies demonstrated that My4 (an antibody blocking the interaction between LPS/LBP and CD14), SB203580, (a specific inhibitor of p38alpha mitogen-activated protein kinase phosphorylation), dexamethasone, and the messenger RNA translation inhibitor cycloheximide all inhibited LPS-induced IL-6 production by TtT/GF cells and mouse pituitary FS cells. LPS-induced intrapituitary IL-6 may modulate the function of anterior pituitary cells during bacterial infection/inflammation.

 

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