Mice lacking both G-CSF and IL-6 are more susceptible to Candida albicans infection: Critical role of neutrophils in defense against Candida albicans

Author: Basu Sunanda   Quilici Cathy   Zhang Hui-Hua   Grail Dianne   Dunn Ashley  

Publisher: Informa Healthcare

ISSN: 0897-7194

Source: Growth Factors, Vol.26, Iss.1, 2008-03, pp. : 23-34

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

Previous Menu Next

Abstract

Neutrophils play an important role in the host's defense against infection with various pathogenic organisms. Granulocyte colony stimulating factor (G-CSF) is regarded as a major regulator of neutrophil production and function. Mice lacking G-CSF or its receptor are neutropenic. IL-6 is another cytokine that has been shown to promote neutrophil production and modulate the function of many types of immune cells. We have analyzed G-CSF/IL-6 double deficient (G-CSF- / - /IL-6- / - ) mice to gain an insight into the possible contribution of IL-6 to the residual granulopoiesis in G-CSF-deficient (G-CSF- / - ) mice. Furthermore, we have evaluated the ability of G-CSF- / - /IL-6- / - mice to combat an experimental infection with Candida albicans. Our data shows that IL-6 plays a role in granulopoiesis during early post natal period but it is dispensable for steady-state granulopoiesis in adult mice. However, adult G-CSF- / - /IL-6- / - mice are more susceptible to Candida infection than similarly infected G-CSF- / - mice. Although, the candidacidal function of neutrophils of G-CSF- / - /IL-6- / - mice is deficient, the ability to produce IFN-γ and TNF-α in response to Candida infection is not compromised. Similarly, nitric oxide production by peritoneal macrophages from G-CSF- / - /IL-6- / - mice in response to Candida is comparable to G-CSF- / - mice.