Danger- and pathogen-associated molecular patterns recognition by pattern-recognition receptors and ion channels of the transient receptor potential family triggers the inflammasome activation in immune cells and sensory neurons.

An increasing number of studies show that the activation of the innate immune system and inflammatory mechanisms play an important role in the pathogenesis of numerous diseases. The innate immune system is present in almost all multicellular organisms and its activation occurs in response to pathogens or tissue injury via pattern-recognition receptors (PRRs) that recognize pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs). Intracellular pathways, linking immune and inflammatory response to ion channel expression and function, have been recently identified. Among ion channels, the transient receptor potential (TRP) channels are a major family of non-selective cation-permeable channels that function as polymodal cellular sensors involved in many physiological and pathological processes.In this review, we summarize current knowledge of interactions between immune cells and PRRs and ion channels of TRP families with PAMPs and DAMPs to provide new insights into the pathogenesis of inflammatory diseases. TRP channels have been found to interfere with innate immunity via both nuclear factor-kB and procaspase-1 activation to generate the mature caspase-1 that cleaves pro-interleukin-1ß cytokine into the mature interleukin-1ß.Sensory neurons are also adapted to recognize dangers by virtue of their sensitivity to intense mechanical, thermal and irritant chemical stimuli. As immune cells, they possess many of the same molecular recognition pathways for danger. Thus, they express PRRs including Toll-like receptors 3, 4, 7, and 9, and stimulation by Toll-like receptor ligands leads to induction of inward currents and sensitization in TRPs. In addition, the expression of inflammasomes in neurons and the involvement of TRPs in central nervous system diseases strongly support a role of TRPs in inflammasome-mediated neurodegenerative pathologies. This field is still at its beginning and further studies may be required.Overall, these studies highlight the therapeutic potential of targeting the inflammasomes in proinflammatory, autoinflammatory and metabolic disorders associated with undesirable activation of the inflammasome by using specific TRP antagonists, anti-human TRP monoclonal antibody or different molecules able to abrogate the TRP channel-mediated inflammatory signals

Measurement of the branching fraction, polarization, and CP asymmetries in B-0 ->rho(0)rho(0) decay, and implications for the CKM angle alpha

We study B-0 ->rho(0)rho(0) decays in a sample of 465x10(6) Upsilon(4S)-> B(B)overbar events collected with the BABAR detector at the PEP-II asymmetric-energy e(+)e(-) collider located at the Stanford Linear Accelerator Center (SLAC). We measure the branching fraction B=(0.92 +/- 0.32 +/- 0.14)x10(-6) and longitudinal polarization fraction f(L)=0.75(-0.14)(+0.11)+/- 0.05, where the first uncertainty is statistical and the second is systematic. The evidence for the B-0 ->rho(0)rho(0) signal has a significance of 3.1 standard deviations, including systematic uncertainties. We investigate the proper-time dependence of the longitudinal component in the decay and measure the CP-violating coefficients S-L(00)=(0.3 +/- 0.7 +/- 0.2) and C-L(00)=(0.2 +/- 0.8 +/- 0.3). We study the implication of these results for the unitarity triangle angle alpha