The Journal of Infectious Diseases · 1995 · 55 citations · 27 references
Veterinary MedicineInfectious DiseasesMicrobiologyHost-pathogen InteractionsImmunology Of Infectious DiseasesMedical MicrobiologyBacterial InfectionsBacterial PathogenesisCentral Nervous System InfectionsInfectious Disease PathophysiologyPathogenesis Of Infectious DiseaseSusceptibility To InfectionHaemophilus Influenzae Type B DiseaseHematogenous InfectionImmune Response To Bacterial InfectionImmunopathogenesis Of Bacterial InfectionInflammatory Response To Bacterial InfectionIntercellular Adhesion Molecule 1Meningeal Immune Responses To InfectionPathogenesis Of Animal Pathogens
Mice genetically deficient in the gene encoding for intercellular adhesion molecule-1 (ICAM-1) production were compared with wild-type mice after injection with Haemophilus influenzae type b (Hib) or Streptococcus pneumoniae. The incidence of Hib bacteremia was greater in the ICAM-1-deficient mice than wild-type mice (P = .007), but mortality was greater for wild-type mice at 24 h (P = .03). In contrast, the incidence of S. pneumoniae bacteremia was equivalent but mortality was greater in ICAM-1-deficient mice at 24 h (P = .0003). More ICAM-1-deficient mice had cerebrospinal fluid cultures (CSF) positive for Hib (P = .04), whereas all animals at sacrifice had CSF cultures positive for S. pneumoniae. CSF white blood cell counts and histology of the meninges and cochlea were no different between groups for either organism. ICAM-1 deficiency may be protective early in Hib infection but has a detrimental effect in S. pneumoniae infection.
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