About: Otitis media (OM) and sinusitis are common and costly maladies that are often preceded by the development of a viral upper respiratory infection (vURI). Although antibiotics have been shown to be somewhat effective in the treatment of these disorders, increasing concern over the emergence of pathogen resistence to these agents underscores the need for the development of other treatment options, including agents to treat and/or prevent vURIs. Earlier research implicated roles for cytopathology, cellular infiltration, and inflammatory mediators such as bradykinin, in the pathogenesis of vURIs and its complications, including OM and sinusitis, but these factors are now recognized as late events with specific and limited contributions to disease expression. Current therapies are relatively ineffective and aimed at reducing symptoms rather than moderating underlying mechanisms. Nasal elevations of proinflammatory cytokines and leukotrienes track symptom expression during vURIs, and it is hypothesized that these chemicals orchestrate a common response to infection with many different viruses causing vURIs. Moreover, recent evidence demonstrates that specific cytokine gene polymorphisms may modulate the severity of illness and incidence of complications during episodes of vURI. Additionally, other evidence supports a role for neurogenic inflammation in the development of complications. Future studies should dissect the role of proinflammatory cytokines, leukotrienes, and neuropeptides in the expression of symptoms, signs, pathophysiologies, and complications of vURIs.   Goto Sponge  NotDistinct  Permalink

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  • Otitis media (OM) and sinusitis are common and costly maladies that are often preceded by the development of a viral upper respiratory infection (vURI). Although antibiotics have been shown to be somewhat effective in the treatment of these disorders, increasing concern over the emergence of pathogen resistence to these agents underscores the need for the development of other treatment options, including agents to treat and/or prevent vURIs. Earlier research implicated roles for cytopathology, cellular infiltration, and inflammatory mediators such as bradykinin, in the pathogenesis of vURIs and its complications, including OM and sinusitis, but these factors are now recognized as late events with specific and limited contributions to disease expression. Current therapies are relatively ineffective and aimed at reducing symptoms rather than moderating underlying mechanisms. Nasal elevations of proinflammatory cytokines and leukotrienes track symptom expression during vURIs, and it is hypothesized that these chemicals orchestrate a common response to infection with many different viruses causing vURIs. Moreover, recent evidence demonstrates that specific cytokine gene polymorphisms may modulate the severity of illness and incidence of complications during episodes of vURI. Additionally, other evidence supports a role for neurogenic inflammation in the development of complications. Future studies should dissect the role of proinflammatory cytokines, leukotrienes, and neuropeptides in the expression of symptoms, signs, pathophysiologies, and complications of vURIs.
Subject
  • Virology
  • Immunology
  • Nose
  • Membrane biology
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