ArticleImmunology2005
Resistance to chlamydial lung infection is dependent on major histocompatibility complex as well as non-major histocompatibility complex determinants.
Article in Immunology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Differences in innate immune responses correlate with differences in murine susceptibility to Chlamydia muridarum pulmonary infection.Immunology · 2010Article
- Critical role of the interleukin-17/interleukin-17 receptor axis in regulating host susceptibility to respiratory infection with Chlamydia species.Infection and immunity · 2009Article
- Sex differences in the genetic architecture of susceptibility to Cryptococcus neoformans pulmonary infection.Genes and immunity · 2008Article
- Genetic control of susceptibility to pulmonary infection with Chlamydia pneumoniae in the mouse.Genes and immunity · 2008Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous work has shown that C3H/HeN and C57BL/6 mice have differential susceptibility to Chlamydia trachomatis mouse pneumonitis (C. muridarum) lung infection. C3H/HeN (H-2(k)) mice were found to be highly susceptible to C. muridarum infection with higher mortality and more severe morbidity compared to C57BL/6 (H-2(b)) mice. To examine the role of major histocompatibility complex (MHC) genes on host resistance to chlamydial lung infection, we compared MHC congenic mice, B6.H2k [C57BL/6 background, C3H MHC (H-2(k))] and C3H.H2b [C3H/HeN background, C57BL/6 MHC (H-2(b))] and their corresponding wild type C57BL/6 mice and C3H/HeN mice, respectively, in susceptibility to C. muridarum infection. We found that B6.H2k, C3H.H2b and C3H/HeN mice are more susceptible to chlamydial lung infection compared to the wild type C57BL/6 mice by showing more serious body weight loss, higher in vivo chlamydial growth and more severe pathologic changes. Congenic B6.H2k mice showed significantly lower levels of IL-12 and IFN-gamma production compared to C57BL/6 as well as C3H/HeN and C3H.H2b mice. One the other hand, although congenic C3H.H2b mice displayed similar cytokine response to C57BL/6 mice, they were highly susceptible to C. muridarum infection. Overall, the results suggest that protection against chlamydial lung infection is both MHC and non-MHC gene dependent, and that the interaction between MHC and non-MHC elements may contribute to host resistance to chlamydial infection.
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