Effect of interferon gamma and CD40 ligation on intracellular monocyte survival of nontypeableHaemophilus influenzae
- Resource Type
- Authors
- Roy M. Robins-Browne; Stephen R. Holdsworth; Frances Oppedisano; James Ngui; Paul T. King; Peter Holmes
- Source
- APMIS. 116:1043-1049
- Subject
- Adult
Male
Microbiology (medical)
Haemophilus Infections
medicine.medical_treatment
CD40 Ligand
Dose-Response Relationship, Immunologic
Biology
medicine.disease_cause
Monocytes
Pathology and Forensic Medicine
Haemophilus influenzae
Microbiology
Interferon-gamma
Immunity
otorhinolaryngologic diseases
medicine
Humans
Immunology and Allergy
Interferon gamma
Cells, Cultured
CD40
Monocyte
Respiratory infection
General Medicine
Middle Aged
Th1 Cells
medicine.anatomical_structure
Cytokine
Immunology
biology.protein
Female
Intracellular
medicine.drug
- Language
- ISSN
- 1600-0463
0903-4641
Nontypeable Haemophilus influenzae (NTHi) is a mucosal pathogen that is a major cause of respiratory infection, including sinusitis, otitis media and bronchitis. This bacterium has evolved a number of mechanisms to facilitate its survival in the human host. Recently it has been recognized that it is capable of intracellular survival in monocytes/macrophages and epithelial cells. Previous work by the authors has demonstrated that the protective response to NTHi is Th1 predominant. This information led to the hypothesis that the intracellular survival of NTHi in human monocytes may be reduced by two key effector mechanisms of Th1-mediated immunity: interferon gamma and ligation of CD40. This study assessed the effect of interferon gamma and ligation of CD40 on the intracellular survival of NTHi in human monocytes. Responses were studied in monocytes from subjects with bronchiectasis and persistent airway infection with NTHi and compared with control subjects. The results demonstrated that different isolates of NTHi were able to survive inside monocytes. Killing of one strain of NTHi could be enhanced by the addition of interferon gamma and CD40 ligation in both control and bronchiectasis subjects. Other strains were more resistant.