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Based on the results of this meta-analysis, it would appear that an algorithm based on serial PCT measurements would allow a more judicious use of antibiotics than currently occurs during the traditional treatment of patients with infections. PCT-guided antibiotic treatment appears to be safe and may also improve clinical outcome.

The major addictive component of tobacco, nicotine, exerts anti-inflammatory effects in multiple cell types and may benefit neurons in various degenerative disorders, such as Alzheimer's and Parkinson's disease, in which an inflammation-related mechanism is implicated. Among the various nicotinic acetylcholine receptors, α7, which has been identified in both neurons and immune cells and has high permeability to calcium, is believed to contribute significantly to nicotinic anti-inflammatory and neuron-protective effects. Although nicotine has been used in clinical trials for the treatment of some inflammatory diseases such as ulcerative colitis, the molecular mechanisms of its actions are largely unknown. In this review, we provide current evidence for nicotine's modulation of multiple immune pathways via α7 nAChRs in both neurons and immune cells. Understanding the mechanism of the nicotinic anti-inflammatory effect and neuron-protective function may guide the development of novel medicines for infectious and neuron-degenerative diseases.

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Cigarette smoking is the major cause of preventable death and morbidity throughout the world. Many compounds are present in tobacco, but nicotine is the primary addictive one. Nicotine exerts its physiological and pharmacological roles in the brain through neuronal nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels consisting of five membrane-spanning subunits that can modulate the release of neurotransmitters, such as dopamine, glutamate, and GABA and mediate fast signal transmission at synapses. Considering that there are 12 nAChR subunits, it is highly likely that subunits other than α4 and β2, which have been intensively investigated, also are involved in nicotine addiction. Consistent with this hypothesis, a number of genome-wide association studies (GWAS) and subsequent candidate gene-based associated studies investigating the genetic variants associated with nicotine dependence (ND) and smoking-related phenotypes have shed light on the CHRNA5/A3/B4 gene cluster on chromosome 15, which encodes the α5, α3, and β4 nAChR subunits, respectively. These studies demonstrate two groups of risk variants in this region. The first one is marked by single nucleotide polymorphism (SNP) rs16969968 in exon 5 of CHRNA5, which changes an aspartic acid residue into asparagine at position 398 (D398N) of the α5 subunit protein sequence, and it is tightly linked SNP rs1051730 in CHRNA3. The second one is SNP rs578776 in the 3'-untranslated region (UTR) of CHRNA3, which has a low correlation with rs16969968. Although the detailed molecular mechanisms underlying these associations remain to be further elucidated, recent findings have shown that α5* (where "*" indicates the presence of additional subunits) nAChRs located in the medial habenulo-interpeduncular nucleus (mHb-IPN) are involved in the control of nicotine self-administration in rodents. Disruption of α5* nAChR signaling diminishes the aversive effects of nicotine on the mHb-IPN pathway and thereby permits more nicotine consumption. To gain a better understanding of the function of the highly significant genetic variants identified in this region in controlling smoking-related behaviors, in this communication, we provide an up-to-date review of the progress of studies focusing on the CHRNA5/A3/B4 gene cluster and its role in ND.