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Xuchen Zhang, Patty J Lee, Response to Comment on “Cutting Edge: TLR4 Deficiency Confers Susceptibility to Lethal Oxidant Lung Injury”, The Journal of Immunology, Volume 176, Issue 7, April 2006, Page 3857, https://doi.org/10.4049/jimmunol.176.7.3857
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Doctors Kubo and Ishizawa raise two issues regarding our studies demonstrating the increased susceptibility of TLR4−/− hyperoxic lung injury (1). The first issue raised is the fact that C3H/HeJ mice, which have mice to defective TLR4 expression, are resistant to hyperoxia (2), which suggests that TLR4 deficiency should confer resistance rather than susceptibility to hyperoxia. In our hands, we also find C3H/HeJ to be resistant to hyperoxia. However, others have already shown that there are important differences in the pulmonary responses between C3H/HeJ and TLR4−/− mice, such as the responses to ozone and fly ash (3). Genetic analyses of C3H/HeJ mice have identified multiple genes, other than TLR4, that are potentially altered and linked to susceptibility patterns (4, 5). Our recent studies demonstrating the decreased survival of TLR4−/− mice, as well as TLR2/4−/− mice to hyperoxia, further support the concept that TLR-independent pathways may account for the resistant phenotype observed in C3H/HeJ mice (1, 6).
