Cyanobacterial lipopolysaccharides and human health – a review

Cyanobacterial lipopolysaccharide/s (LPS) are frequently cited in the cyanobacteria literature as toxins responsible for a variety of heath effects in humans, from skin rashes to gastrointestinal, respiratory and allergic reactions. The attribution of toxic properties to cyanobacterial LPS dates from the 1970s, when it was thought that lipid A, the toxic moiety of LPS, was structurally and functionally conserved across all Gram-negative bacteria. However, more recent research has shown that this is not the case, and lipid A structures are now known to be very different, expressing properties ranging from LPS agonists, through weak endotoxicity to LPS antagonists. Although cyanobacterial LPS is widely cited as a putative toxin, most of the small number of formal research reports describe cyanobacterial LPS as weakly toxic compared to LPS from the Enterobacteriaceae. We systematically reviewed the literature on cyanobacterial LPS, and also examined the much lager body of literature relating to heterotrophic bacterial LPS and the atypical lipid A structures of some photosynthetic bacteria. While the literature on the biological activity of heterotrophic bacterial LPS is overwhelmingly large and therefore difficult to review for the purposes of exclusion, we were unable to find a convincing body of evidence to suggest that heterotrophic bacterial LPS, in the absence of other virulence factors, is responsible for acute gastrointestinal, dermatological or allergic reactions via natural exposure routes in humans. There is a danger that initial speculation about cyanobacterial LPS may evolve into orthodoxy without basis in research findings. No cyanobacterial lipid A structures have been described and published to date, so a recommendation is made that cyanobacteriologists should not continue to attribute such a diverse range of clinical symptoms to cyanobacterial LPS without research confirmation

[Metabolic stability and physiological adaptation of muscle under conditions of exercise]

The first role played by group III (thin myelinated) and group IV (unmyelinated) afferent fibres from skeletal muscle is to transmit nociceptive information from muscle to the central nervous system. The second role of these free endings located in the interstitium of the muscle is to induce cardiovascular and respiratory adjustments during muscular exercise. These respiratory and circulatory responses during muscular exercise may be reflexly induced via muscular afferents. Indeed, static contraction of hindlimb muscles in anaesthetised mammals has been shown to reflexly increase the ventilatory function, the myocardial contractility and heart rate. The mechanical muscle deformation and the accumulation of metabolites in its intersitium are the cause of raised activity in small nerve fibres which in turn induces the physiological responses. It is also admitted that the central locomotor areas on the medullary and spinal neuronal pools control ventilatory and cardiovascular function during exercise. This mechanism is called "central command". Furthermore, adjustments of the locomotor activity during exercise is mediated by the thinly myelinated and unmyelinated fibres with endings in the working muscle. These fibres, also called "metaboreceptor" may be responsible of the coupling between the ventilation and the locomotion. Thickly myelinated muscle afferents (i.e. group I and II) appear to play little role in causing the reflex autonomic responses to contraction

Comparison between the effects of chronic and acute hypoxemia on muscle afferent activities from the tibialis anterior muscle

International audienceThe reflex loops initiated by the activation of muscle afferents are altered by a reduction of the oxygen supply. This has been shown in different mammalian species under experimental conditions of acute or chronic hypoxemia. In the present study in rats, we compared the effects of acute and chronic hypoxemia on the activity of afferents from the tibialis anterior muscle to investigate the existence of possible adaptive mechanisms to hypoxaemia. The activity in groups I and II (mechanosensitive) and groups III and IV (mechano- and mostly chemosensitive) muscle afferents was recorded under conditions of normoxaemia and acute and chronic hypoxemia. Chronic hypoxaemia was achieved by exposing the rats for 45 consecutive days to a gas mixture containing 10% oxygen in nitrogen, whereas acute hypoxaemia was limited to a 1-h exposure to a 10% oxygen mixture. Different test agents: muscle stimulation (MS), arterial injection of KCl or lactic acid and tendon vibrations, were used to activate muscle afferents. Both acute and chronic hypoxaemia suppressed the post-MS activation of groups III and IV muscle afferents and significantly depressed the response of these afferents to KCl and lactic acid. The pattern of response of mechanosensitive afferents to mechanical tendon vibration was similar under the three conditions but chronic hypoxemia significantly reduced the response to 10-50 Hz vibrations. We conclude that inhibitory effects on muscle metabosensitive afferents occurred in the first minutes following acute hypoxemia and was prolonged with chronic hypoxemia. Our data also suggest that chronic hypoxemia depresses mechanosensitive muscle afferents. This may explain the observation that sensorimotor control of skeletal muscles is often markedly impaired in hypoxemic humans

Détermination par l'IRM et l'EMG des muscles impliqués dans le pédalage chez les cyclistes professionnels

Hug François, Bendahan David, Savin B., Cozzone Patrick, Grélot Laurent. Détermination par l'IRM et l'EMG des muscles impliqués dans le pédalage chez les cyclistes professionnels. In: Les Cahiers de l'INSEP, n°34, 2003. Expertise et sport de haut niveau. pp. 397-401

Effects of chronic hypoxemia on the afferent nerve activities from skeletal muscle

International audienceAn acute reduction of the oxygen supply to contracting muscles not only affects their metabolism but also modifies their sensorimotor control through changes in afferent discharge of the group I and group III-IV nerve fibers, the latter playing a pivotal role in the protective mechanisms against muscle fatigue. The effects of chronic hypoxemia on the muscle sensitivity are totally unknown. In the present study, group I fibers (mechanosensory afferents) and group III-IV fibers (mechanosensory and chemosensory afferents) from the anterior tibial muscle were recorded in normoxemic and chronic hypoxemic rats. Hypoxemic rats breathed for 45 d a gas mixture containing 9.5 to 10% O(2) in N(2). The data were compared with those obtained in normoxemic animals of the same age. To activate the different muscle afferents, we used different test agents, including electrically induced fatigue (EIF), KCl, lactic acid injections, as well as tendon vibrations. The conduction velocity of all nerve fibers was significantly (p \textless 0.01) higher in hypoxemic rats than in the normoxemic group. Chronic hypoxemia significantly depressed the response of the group III-IV muscle afferents to KCl injections and even abolished their response to lactic acid and EIF. However, the response to tendon vibrations of the group I afferents was similar in hypoxemic and normoxemic rats. These results suggest that chronic hypoxemia markedly alters the chemosensitivity of the group III-IV muscle afferents, which may explain the higher fatigability of hypoxemic subjects

Potent inhibition of both the acute and delayed emetic responses to cisplatin in piglets treated with GR205171, a novel highly selective tachykinin NK(1) receptor antagonist

1. The effects of GR205171, a selective tachykinin NK(1) receptor antagonist, were investigated on both the acute and delayed phases of cisplatin-induced nausea-like behaviour and vomiting in the conscious piglet. 2. Animals receiving cisplatin (5.5 mg kg(−1), i.v.) were observed for 60 h. Fifteen min prior to cisplatin infusion (T0(−15 min)), eight piglets acting as controls received an intravenous injection of saline solution (1 ml kg(−1)), whereas experimental animals received a single i.v. administration of GR205171 (1 ml kg(−1)) at a dose of 0.01 (n=8), 0.03 (n=8), 0.1 (n=8), 0.3 (n=16) or 1.0 (n=13) mg kg(−1). In eight additional piglets, GR205171 (1 mg kg(−1)) was administered 15 min before the onset of the delayed phase (T16(−15 min)). A further five piglets received GR205171 (1 mg kg(−1)) every 6 h throughout the experiment. 3. The latencies of the first emetic episode (EE) and nausea-like behavioural episode (NE) increased in all experimental groups treated at T0(−15 min), and the total number of both EE and NE during the 60 h was reduced in a dose-dependent manner. In piglets treated at T0(−15 min) with GR205171 1 mg kg(−1), eight out of 13 (62%) did not vomit throughout the experiment. Animals treated with GR205171 (1 mg kg(−1)) at T16(−15 min) exhibited an acute response to cisplatin but did not vomit during the delayed phase. The greatest inhibition of both nausea-like behaviour and vomiting was observed in piglets receiving multiple injections of GR205171. 4. These results demonstrate the long-lasting anti-emetic effects of GR205171, and confirm the key role of substance P within the emetic reflex