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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We presented a case of critical illness polyneuropathy after bacterial peritonitis. A 62-year-old male was received an emergency colectomy because of perforation of the sigmoid colon five days after the endoscopic polypectomy. He developed sepsis from peritonitis after operation in spite of the antibiotics therapy. On 15-th hospital days he developed muscle weakness and numbness of all limbs. He needed an artificial ventilator due to respiratory failure. Hematological and blood chemical findings showed a leukocytosis and metabolic acidosis with renal dysfunction because of sepsis. Serum anti-Campylobacter antibody was negative. Serial CSF examinations failed to show any abnormalities including albuminocytologic dissociation. Electrophysiological studies revealed a primary axonal degeneration, mainly in the motor, but also in the sensory nerve. Compound muscle and sensory action potentials were not elicited or markedly reduced without conduction velocity prolongation. Microscopic findings of the left sural nerve biopsy showed a primary axonal degeneration without evidence of inflammation. His prognosis was poor and three months later, he still required ventilatory assistance. Because of these clinical findings this patient was thought to have a critical illness polyneuropathy after excluding various etiologies of polyneuropathies. This case suggests that sepsis may be one of a cause of primary axonal polyneuropathy. The certain mechanism of this disease is still unknown. However cytokine, tumor necrotic factor(TNF) and/or Platelet activating factor(PAF) that secreted during sepsis may have an important role for the primary axonal degeneration.
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PMID:[A case of critical illness polyneuropathy in association with peritonitis after sigmoid colon perforation]. 766 19

The aim was to study in vitro regulation of the IL-5 receptor alpha (IL-5R alpha) on purified peripheral blood eosinophils from healthy subjects. The IL-5R alpha was down-regulated, in a dose-dependent manner, by recombinant IL-5 and GM-CSF, with IL-5 being most potent. This down-regulation was not induced by autocrine release of GM-CSF or IL-5, respectively. Incubation of eosinophils with cell-free peritoneal dialysis fluid (PF) collected from a patient with peritoneal fluid eosinophilia (PFE), induced up-regulation of the proportion of CD69 positive eosinophils, in parallel with down-regulation of the proportion of IL-5R alpha positive eosinophils. Experiments with neutralizing antibodies against IL-5 and GM-CSF, revealed that IL-5 was the principal cytokine responsible for the down-regulation of the IL-5R alpha. When eosinophils were incubated with PF collected from the same patient in remission or with PF collected from a newly started patient or a patient with bacterial peritonitis, less down-regulation of the IL-5R alpha was observed. In conclusion our data indicate that IL-5, as opposed to its proposed action on eosinophil progenitors, down-regulates the IL-5R alpha chain on mature eosinophils. We therefore suggest that an IL-5 driven inflammation generates an eosinophil tissue phenotype that is characterized by a low IL-5R alpha expression. These aspects of IL-5 action on IL-5R alpha expression could gain new insights into the mechanisms of specific immuno-modulatory therapies, such as anti-IL-5.
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PMID:Regulation of the interleukin-5 receptor alpha-subunit on peripheral blood eosinophils from healthy subjects. 1251 89

Granulocyte-macrophage-colony-stimulating factor (GM-CSF) plays a critical role in innate immunity by stimulating the differentiation of tissue macrophages via the transcription factor PU.1. Previous studies showed that GMCSF-deficient(GM-CSF-/-) mice had susceptibility to and impaired clearance of group B streptococcal bacteria by macrophages. For these studies, we hypothesized that GM-CSF-/- mice have increased susceptibility to peritonitis caused by immune dysfunction of peritoneal macrophages. We examined the role of peritoneal macrophages in pathogen clearance, cytokine responses, and survival in a murine cecal ligation and puncture (CLP) model of peritonitis/sepsis. Surprisingly, CLP minimally affected survival in GM-CSF-/- mice while markedly reducing survival in wild-type mice. This was not explained by differences in the composition of microbial flora, rates of bacterial peritonitis, or sepsis, all of which were similar in GM-CSF-/- and wild-type mice. However, survival correlated with peritoneal and serum TNF-alpha and IL-6 levels that were significantly lower in GM-CSF-/- than in control mice. After peritoneal LPS instillation, GM-CSF-/- mice also had improved survival and reduced TNF-alpha and IL-6 responses. In vitro studies demonstrated reduced secretion of TNF-alpha and IL-6 by peritoneal macrophages isolated from sham GM-CSF-/- mice as compared with macrophages from sham control mice. Peritoneal instillation of GM-CSF-/-/PU.1+ macrophages, but not GM-CSF-/-/PU.1+ macrophages into GM-CSF-/- mice conferred susceptibility to death after CLP or peritoneal LPS exposure. These results demonstrate that GM-CSFY/PU.1-dependent peritoneal macrophage responses are a critical determinant of survival after experimentally induced peritonitis/sepsis or exposure to LPS and have implications for therapies to treat such infections.
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PMID:Granulocyte-macrophage-colony-stimulating factor-dependent peritoneal macrophage responses determine survival in experimentally induced peritonitis and sepsis in mice. 1827 45