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Infectivity of Borrelia burgdorferi sensu lato is unaltered in C3-deficient mice
N D van Burgel1, N C M Balmus, E Fikrig
1Dept. of Medical Microbiology, Centre of Infectious Diseases, Leiden University Medical Centre, PO Box 9600, 2300 RC Leiden, The Netherlands. N.D.van Burgel@LUMC.nl
Abstract:
B. burgdorferi, B. afzelii, and B. bavariensis show resistance to mouse and human complement. B. garinii and B. valaisiana are sensitive to mouse and human complement. We evaluated whether the absence of C3 in mice influenced infectivity and pathogenicity of different Borrelia species. C3 knockout mice (C3-/-) and syngeneic C57Bl/6 wild-type (WT) mice were challenged with 5 different Borrelia species. After 2 weeks, quantitative PCR (qPCR), culture, histopathology, and immunofluorescence were performed on heart, joint, brain, bladder, and skin. Spirochaetes were detected by qPCR after infection with B. burgdorferi, B. afzelii, or B. bavariensis strains. In joints of C3-/-, but not WT mice challenged with B. burgdorferi, spirochaetes were detected by qPCR. No other significant differences between C3-/- and WT mice were seen. Histopathology demonstrated concordance between borrelia load and inflammation score. Only after B. burgdorferi and B. afzelii infection, spirochaetes were detected by immunofluorescence microscopy. B. burgdorferi was cultured from heart, joint, bladder, and skin from all mice within 2 weeks. B. afzelii and B. bavariensis grew only from heart tissue from both C3-/- and WT mice after 2-6 weeks. The infectivity and pathogenicity of complement-resistant Borrelia strains is unchanged in complement-deficient mice. Complement-susceptible strains do not become infectious in the absence of C3.
Insights
Complement deficiency in mice did not alter the infectivity of complement-resistant Borrelia species. Complement-susceptible Borrelia strains did not become infectious in C3 knockout mice, indicating complement
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Borrelia species exhibit variable resistance to host complement.
- Complement component 3 (C3) plays a crucial role in innate immunity against bacterial pathogens.
Purpose of the Study:
- To investigate the impact of C3 deficiency on the infectivity and pathogenicity of different Borrelia species in mice.
- To determine if complement resistance influences Borrelia pathogenesis in the absence of C3.
Main Methods:
- Comparison of C3 knockout (C3-/-) and wild-type (WT) mice challenged with five Borrelia species.
- Detection of spirochaetes using quantitative PCR (qPCR), culture, histopathology, and immunofluorescence microscopy.
- Analysis of various tissues including heart, joint, brain, bladder, and skin.
Main Results:
- Complement-resistant Borrelia species (B. burgdorferi, B. afzelii, B. bavariensis) showed similar infectivity and pathogenicity in both C3-/- and WT mice.
- Complement-susceptible Borrelia species (B. garinii, B. valaisiana) did not become infectious in C3-/- mice.
- Spirochaetes were detected in joints of C3-/- mice infected with B. burgdorferi, but not in WT mice.
- B. burgdorferi was culturable from multiple tissues in both mouse groups; B. afzelii and B. bavariensis were primarily cultured from heart tissue.
Conclusions:
- The absence of C3 does not enhance the infectivity or pathogenicity of complement-resistant Borrelia strains.
- Complement-susceptible Borrelia strains are unable to establish infection in C3-deficient mice.
- Host complement, specifically C3, is critical for the initial infection by complement-susceptible Borrelia species.
