Giuseppe
Emeritus
Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection (BioMedCentral, abstract, edited)
[Source: BioMed Central, full text: <cite cite="http://www.biomedcentral.com/1471-2172/11/64/abstract">Abstract | Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection</cite>. Abstract, edited.]
Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection
Wei-Chuan Chang, Mitchell R. White, Patience Moyo, Sheree McClear, Steffen Thiel, Kevan L. Hartshorn and Kazue Takahashi
BMC Immunology 2010, 11:64
doi:10.1186/1471-2172-11-64
Published: 23 December 2010
Abstract (provisional)
Background
Mannose-binding lectin (MBL), a pattern recognition innate immune molecule, inhibits influenza A virus infection in vitro. MBL deficiency due to gene polymorphism in humans has been associated with infection susceptibility. These clinical observations were confirmed by animal model studies, in which mice genetically lacking MBL were susceptible to certain pathogens, including herpes simplex virus 2.
Results
We demonstrate that MBL is present in the lung of naive healthy wild type (WT) mice and that MBL null mice are more susceptible to IAV infection. Administration of recombinant human MBL (rhMBL) reverses the infection phenotype, confirming that the infection susceptibility is MBL-mediated. The anti-viral mechanisms of MBL include activation of the lectin complement pathway and coagulation, requiring serum factors. White blood cells (WBCs) in the lung increase in WT mice compared with MBL null mice on day 1 post-infection. In contrast, apoptotic macrophages (MPhis) are two-fold higher in the lung of MBL null mice compared with WT mice. Furthermore, MBL deficient macrophages appear to be susceptible to apoptosis in vitro. Lastly, soluble factors, which are associated with lung injury, are increased in the lungs of MBL null mice during IAV infection. These results suggest that MBL plays a key role against IAV infection.
Conclusion
MBL plays a key role in clearing IAV and maintaining lung homeostasis. In addition, our findings also suggest that MBL deficiency maybe a risk factor in IAV infection and MBL may be a useful adjunctive therapy for IAV infection.
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[Source: BioMed Central, full text: <cite cite="http://www.biomedcentral.com/1471-2172/11/64/abstract">Abstract | Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection</cite>. Abstract, edited.]
Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection
Wei-Chuan Chang, Mitchell R. White, Patience Moyo, Sheree McClear, Steffen Thiel, Kevan L. Hartshorn and Kazue Takahashi
BMC Immunology 2010, 11:64
doi:10.1186/1471-2172-11-64
Published: 23 December 2010
Abstract (provisional)
Background
Mannose-binding lectin (MBL), a pattern recognition innate immune molecule, inhibits influenza A virus infection in vitro. MBL deficiency due to gene polymorphism in humans has been associated with infection susceptibility. These clinical observations were confirmed by animal model studies, in which mice genetically lacking MBL were susceptible to certain pathogens, including herpes simplex virus 2.
Results
We demonstrate that MBL is present in the lung of naive healthy wild type (WT) mice and that MBL null mice are more susceptible to IAV infection. Administration of recombinant human MBL (rhMBL) reverses the infection phenotype, confirming that the infection susceptibility is MBL-mediated. The anti-viral mechanisms of MBL include activation of the lectin complement pathway and coagulation, requiring serum factors. White blood cells (WBCs) in the lung increase in WT mice compared with MBL null mice on day 1 post-infection. In contrast, apoptotic macrophages (MPhis) are two-fold higher in the lung of MBL null mice compared with WT mice. Furthermore, MBL deficient macrophages appear to be susceptible to apoptosis in vitro. Lastly, soluble factors, which are associated with lung injury, are increased in the lungs of MBL null mice during IAV infection. These results suggest that MBL plays a key role against IAV infection.
Conclusion
MBL plays a key role in clearing IAV and maintaining lung homeostasis. In addition, our findings also suggest that MBL deficiency maybe a risk factor in IAV infection and MBL may be a useful adjunctive therapy for IAV infection.
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