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Passive Administration of Monoclonal Antibodies Against H. capsulatum and Others Fungal Pathogens
Published on: February 14, 2011
Anti-CD11 b monoclonal antibody suppresses brain dissemination of Cryptococcus neoformans in mice
Kazuyoshi Kawakami1, Yoshinobu Koguchi, Mahboob Hossain Qureshi
1First Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan. kawakami@med.u-ryukyu.ac.jp
Abstract:
To elucidate the role of the beta2 integrin family of adhesion molecules in the disseminated infection of Cryptococcus neoformans from the lung to the central nervous system, we examined the effects of monoclonal antibodies (mAbs) against CD11a, CD11b, CD11c and CD18 on the number of live microorganisms in both the lung and brain of mice three weeks after intratracheal infection. Administration of anti-CD11b mAb partially, but reproducibly, reduced the fungal loads in the brain in three independent experiments, while the lung loads were not affected. In addition, the same treatment significantly decreased the number of live microorganisms in the blood. In sharp contrast, the brain loads one week after intravenous injection with C. neoformans were not affected by treatment with anti-CD11b mAb. Finally, administration of mAb against other adhesion molecules (CD11a, CD11c or CD18) failed to affect the fungal loads in the brain as well as in the lung three weeks after intratracheal instillation, except for anti-CD18 mAb which rather increased the brain loads. Our results suggested that CD11b might be involved at least in part in the process of fungal dissemination from lung to brain, although the significance of other beta2 integrin family adhesion molecules remains to be substantiated.
Insights
The beta2 integrin CD11b plays a role in Cryptococcus neoformans dissemination from the lung to the brain in mice. Targeting CD11b reduced fungal loads in the brain and blood, but not the lung.
Area of Science:
- Immunology
- Infectious Diseases
- Microbiology
Background:
- Disseminated fungal infections, such as Cryptococcus neoformans, pose significant health risks.
- Adhesion molecules, particularly beta2 integrins, are crucial for immune cell interactions and pathogen dissemination.
- Understanding the role of specific adhesion molecules in fungal spread is vital for developing targeted therapies.
Purpose of the Study:
- To investigate the involvement of beta2 integrin family adhesion molecules (CD11a, CD11b, CD11c, CD18) in the dissemination of Cryptococcus neoformans from the lung to the central nervous system.
- To determine the effect of monoclonal antibodies targeting these molecules on fungal loads in the lung, brain, and blood of infected mice.
Main Methods:
- Mice were intratracheally infected with Cryptococcus neoformans.
- Monoclonal antibodies against CD11a, CD11b, CD11c, and CD18 were administered.
- Fungal loads in the lung, brain, and blood were quantified three weeks post-infection.
- Additionally, the effect of anti-CD11b mAb was assessed after intravenous C. neoformans injection.
Main Results:
- Administration of anti-CD11b monoclonal antibody significantly reduced fungal loads in the brain and blood, but not in the lung, following intratracheal infection.
- This treatment did not affect brain fungal loads when infection was established via intravenous injection.
- Monoclonal antibodies against CD11a, CD11c, and CD18 did not significantly alter fungal loads in the lung or brain, with anti-CD18 mAb treatment paradoxically increasing brain fungal burden.
Conclusions:
- The beta2 integrin CD11b appears to be partially involved in the dissemination of Cryptococcus neoformans from the lung to the brain.
- Other beta2 integrin family members' roles in this dissemination process require further investigation.
- Targeting CD11b may represent a potential therapeutic strategy to limit fungal neuroinvasion.
