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Published ahead of print on September 25, 2002, doi:10.1164/rccm.200207-698OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 2, January 2003, 171-179

A more recent version of this article appeared on January 15, 2003
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Submitted on July 15, 2002
Accepted on September 18, 2002

Alveolar Macrophages have a Protective Anti-Inflammatory Role during Murine Pneumococcal Pneumonia

Sylvia Knapp1*, Jaklien C Leemans1, Sandrine Florquin2, Judith Branger1, Nico A Maris1, Jennie M Pater1, Nico van Rooijen3, and Tom van der Poll4

1 Laboratory for Experimental Internal Medine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands, 2 Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands, 3 Cell Biology and Immunology, Free University of Amsterdam, Amsterdam, The Netherlands, 4 Laboratory for Experimental Internal Medine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

* To whom correspondence should be addressed. E-mail: s.knapp{at}amc.uva.nl.

Alveolar macrophages (AM) are considered major effector cells in host defense against respiratory tract infections by virtue of their potent phagocytic properties. In addition, AM may regulate the host inflammatory response to infection by production of cytokines and by their capacity to phagocytose apoptotic polymorphonuclear cells (PMN). To elucidate the in vivo contribution of AM to host defense against pneumococcal pneumonia we depleted mice of AM via pulmonary application of liposomal dichloromethylene-bisphosphonate (AM-mice) before inoculation with Streptococcus pneumoniae; controls received saline (AM+sal) or liposomal PBS (AM+lip) before bacterial inoculation. AM-mice displayed a significantly higher mortality compared to AM+controls whereas bacterial clearance did not differ. Poor outcome of AM-mice was accompanied by a pronounced increase of local pro-inflammatory cytokine production as well as strongly elevated and prolonged pulmonary PMN accumulation. Closer examination of infiltrating PMN in AM-mice disclosed high proportions of apoptotic and secondary necrotic cells reflecting the lack of efficient clearance mechanisms in the absence of AM. Furthermore, caspase-3 staining showed only slightly higher activity in AM-mice, arguing against accelerated apoptosis per se. These data suggest that AM are indispensable in the host response to pneumococcal pneumonia by means of their capacity to modulate inflammation possibly via elimination of apoptotic PMN.
Key words: Bacterial, Lung, Macrophage, Inflammation, Apoptosis




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