Heme-copper oxygen reductases (HCO) reduce O(2) to water being the last enzymatic complexes of most aerobic respiratory chains. These enzymes promote energy conservation coupling the catalytic reaction to charge separation and charge translocation across the prokaryotic cytoplasmatic or mitochondrial membrane. In this way they contribute to the establishment and maintenance of the transmembrane difference of electrochemical potential, which is vital for solute/nutrient cell import, synthesis of ATP and motility. The HCO enzymes most probably share with the nitric oxide reductases, NORs, a common ancestor. We have proposed the classification of HCOs into three different types, A, B and C; based on the constituents of their proton channels (Pereira, Santana and Teixeira (2001) Biochim Biophys Acta, 1505, 185-208). This classification was recently challenged by the suggestion of other different types of HCOs. Using an enlarged sampling we performed an exhaustive bioinformatic reanalysis of HCOs family. Our results strengthened our previously proposed classification and showed no need for the existence of more divisions. Now, we analyze the taxonomic distribution of HCOs and NORs and the congruence of their sequence trees with the 16S rRNA tree. We observed that HCOs are widely distributed in the two prokaryotic domains and that the different types of enzymes are not confined to a specific taxonomic group or environmental niche.

The notion of "immune privilege" of the brain has been revised to accommodate its infiltration, at steady state, by immune cells that participate in normal neurophysiology. However, the immune mechanisms that regulate learning and memory remain poorly understood. Here we show that noninflammatory IL-17 derived from a previously unknown foetal-derived meningeal-resident γδ T cell subset promotes cognition. When tested in classical spatial learning paradigms, mice lacking γδ T cells or IL-17 displayed deficient short-term memory, while retaining long-term memory.

Neuroinflammation in patients with Alzheimer's disease (AD) and related mouse models has been recognized for decades, but the contribution of the recently described meningeal immune population to AD pathogenesis remains to be addressed. Here, using the 3xTg-AD model, we report an accumulation of interleukin-17 (IL-17)-producing cells, mostly gd T cells, in the brain and the meninges of female, but not male, mice, concomitant with the onset of cognitive decline. Critically, IL-17 neutralization into the ventricles is sufficient to prevent short-term memory and synaptic plasticity deficits at early stages of disease. These effects precede blood-brain barrier disruption and amyloid-beta or tau pathology, implying an early involvement of IL-17 in AD pathology. When IL-17 is neutralized at later stages of disease, the onset of short-memory deficits and amyloidosis-related splenomegaly is delayed. Altogether, our data support the idea that cognition relies on a finely regulated balance of ''inflammatory'' cytokines derived from the meningeal immune system.

No abstract

Alternative complex III forms a recently identified family of enzymes with quinol:electron acceptor oxidoreductase activity. First biochemical and genomic analyses showed that ACIII is composed of six to eight subunits, most of which homologous to different proteins or domains already observed in other known enzymatic complexes. The increasing number of completely sequenced genomes led us to perform a new search for the genes coding for the different ACIII subunits. We have identified a larger number of gene clusters coding for ACIII, still confined to the bacterial domain, but extended to classes in which it was not observed before. We also found an unanticipated diversity in gene clusters, both in terms of its constitution and organization. The several unexpected gene arrangements brought new perspectives to the role of the different subunits of ACIII, namely in quinone binding and in proton translocation. This article is part of a Special Issue entitled: Respiratory complex III and related bc complexes.