RESUMO
Animals possess conserved mechanisms to detect pathogens and to improve survival in their presence by altering their own behavior and physiology. Here, we utilize Caenorhabditis elegans as a model host to ask whether bacterial volatiles constitute microbe-associated molecular patterns. Using gas chromatography-mass spectrometry, we identify six prominent volatiles released by the bacterium Pseudomonas aeruginosa. We show that a specific volatile, 1-undecene, activates nematode odor sensory neurons inducing both flight and fight responses in worms. Using behavioral assays, we show that worms are repelled by 1-undecene and that this aversion response is driven by the detection of this volatile through AWB odor sensory neurons. Furthermore, we find that 1-undecene odor can induce immune effectors specific to P. aeruginosa via AWB neurons and that brief pre-exposure of worms to the odor enhances their survival upon subsequent bacterial infection. These results show that 1-undecene derived from P. aeruginosa serves as a pathogen-associated molecular pattern for the induction of protective responses in C. elegans.
Assuntos
Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/fisiologia , Pseudomonas aeruginosa/metabolismo , Animais , Interações Hospedeiro-Patógeno/fisiologia , Odorantes , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/fisiologia , Transdução de Sinais/fisiologiaRESUMO
Hepatitis A is one of the most common causes of acute viral hepatitis in children. Immunological manifestations involving the nervous system are rare with hepatitis A infection. We report a case of a toddler who presented with acute liver failure secondary to hepatitis A infection. The child showed clinical and laboratory improvement initially with conservative management. However, after the initial improvement, she developed acute-onset ptosis along with areflexia. Serological and neurophysiological tests revealed the occurrence of ocular variant Guillain-Barré syndrome and ocular myasthenia gravis, which was only partially responsive to treatment (intravenous immunoglobulin and pyridostigmine). A sudden clinical deterioration was noted after the onset of ptosis. She succumbed on day 40 of hospitalisation due to hospital-acquired infection along with the primary hepatic pathology. This is a rare coincidental presentation of acute viral hepatitis A infection with autoimmune manifestations.