Karen M Dahl

Publications (3)20.45 Total impact

• Article: Regulation of chemokine expression by NaCl occurs independently of cystic fibrosis transmembrane conductance regulator in macrophages.

  Amanda G Kostyk, Karen M Dahl, Murry W Wynes, Laurie A Whittaker, Daniel J Weiss, Roberto Loi, David W H Riches
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  ABSTRACT: Chronic pulmonary inflammation and infection are the leading causes of morbidity and mortality in cystic fibrosis (CF). While the effect of mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) on airways remains controversial, some groups have demonstrated increases in Na(+) and Cl(-) in CF airway surface liquid compared to normal airways. We investigated the consequences of NaCl on pro-inflammatory chemokine and cytokine production by macrophages. Stimulation of mouse macrophages with increasing amounts of NaCl induced macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-alpha (TNF-alpha) production. Further, co-incubation of macrophages with NaCl in the presence of either lipopolysaccharide (LPS) or TNF-alpha synergistically increased MIP-2 production. Both the NaCl and NaCl plus LPS responses were partially dependent on endogenous production and autocrine signaling by TNF-alpha. To investigate the role of CFTR in MIP-2 production, we compared the responses of wild-type and DeltaF508 CF mouse macrophages to NaCl and LPS. The responses of macrophages from both strains were indistinguishable. In addition, CFTR mRNA was not expressed in macrophages. Taken together, these findings suggest that NaCl stimulates MIP-2 production by macrophages through a mechanism that is partially dependent on TNF-alpha but independent of macrophage CFTR expression.
  American Journal Of Pathology 08/2006; 169(1):12-20. · 4.89 Impact Factor
• Article: Development of resistance to acyclovir during chronic infection with the Oka vaccine strain of varicella-zoster virus, in an immunosuppressed child.

  Myron J Levin, Karen M Dahl, Adriana Weinberg, Roger Giller, Amita Patel, Philip R Krause
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  ABSTRACT: A 1-year-old boy was vaccinated with the Oka strain of varicella just prior to the discovery of a tumor that required intensive antitumor therapy. Three months later he developed herpes zoster, which developed into chronic verrucous lesions that were refractory to treatment with acyclovir and which subsequently disseminated. DNA from a biopsy specimen of a chronic herpes-zoster lesion indicated that the Oka vaccine strain of the the virus caused this severe complication. Analysis of this viral DNA demonstrated a mutation in the viral thymidine kinase gene. Plasmids containing this altered gene were unable to produce functional thymidine kinase in an in vitro translation system. The presence of this mutation would explain the clinical resistance to acyclovir. This is the first report of Oka-strain varicella virus causing severe disease after reactivation and of resistance to acyclovir during an infection caused by this virus.
  The Journal of Infectious Diseases 11/2003; 188(7):954-9. · 6.41 Impact Factor
• Article: Escherichia hermannii infection of a cephalohematoma: case report, review of the literature, and description of a novel invasive pathogen.

  Karen M Dahl, James Barry, Roberta L DeBiasi
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  ABSTRACT: We describe a neonate with bacterial infection of a cephalohematoma by Escherichia hermannii and with meningitis. We review the literature on infected cephalohematomas and E. hermannii and document the first case of invasive disease due to this pathogen.
  Clinical Infectious Diseases 12/2002; 35(9):e96-8. · 9.15 Impact Factor