- Stress responses in Streptococcus species and their effects on the host
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Cuong Thach Nguyen , Sang-Sang Park , Dong-Kwon Rhee
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J. Microbiol. 2015;53(11):741-749. Published online October 28, 2015
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DOI: https://doi.org/10.1007/s12275-015-5432-6
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Abstract
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Streptococci cause a variety of diseases, such as dental caries,
pharyngitis, meningitis, pneumonia, bacteremia, endocarditis,
erysipelas, and necrotizing fasciitis. The natural niche of this
genus of bacteria ranges from the mouth and nasopharynx
to the skin, indicating that the bacteria will inevitably be subjected
to environmental changes during invasion into the host,
where it is exposed to the host immune system. Thus, the
Streptococcus-host interaction determines whether bacteria are
cleared by the host’s defenses or whether they survive after
invasion to cause serious diseases. If this interaction was to
be deciphered, it could aid in the development of novel preventive
and therapeutic agents. Streptococcus species possess
many virulent factors, such as peroxidases and heat-shock
proteins (HSPs), which play key roles in protecting the bacteria
from hostile host environments. This review will discuss
insights into the mechanism(s) by which streptococci adapt
to host environments. Additionally, we will address how streptococcal
infections trigger host stress responses; however,
the mechanism by which bacterial components modulate
host stress responses remains largely unknown.
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- Virulence Attenuation of Streptococcus pneumoniae clpP Mutant by Sensitivity to Oxidative Stress in Macrophages via an NO-Mediated Pathway
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Chul-Yong Park , Eun-Hye Kim , Sang-Yoon Choi , Thao Dang-Hien Tran , In-Hye Kim , Su-Nam Kim , Suhkneung Pyo , Dong-Kwon Rhee
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J. Microbiol. 2010;48(2):229-235. Published online May 1, 2010
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DOI: https://doi.org/10.1007/s12275-010-9300-0
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965
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Abstract
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ClpP protease is essential for virulence and survival under stress conditions in several pathogenic bacteria. The clpP mutation in a murine infection model has demonstrated both attenuation of virulence and a sensitivity to hydrogen peroxide. However, the underlying mechanisms for these changes have not been resolved. Because macrophages play a major role in immune response and activated macrophages can kill microbes via oxygen-dependant mechanisms, we investigated the effect of the clpP mutation on its sensitivity to macrophage-mediated oxygen-dependant mechanisms. The clpP mutant derived from D39 (serotype 2) exhibited a higher sensitivity to oxidative stresses such as reactive oxygen intermediates, reactive nitrogen intermediates, and H2O2, but no sensitivity to osmotic stress (NaCl) and pH. Moreover, viability of the clpP mutant was significantly increased in murine macrophage cells by treatment with S-methylisothiourea sulfate, which inhibits inducible nitric oxide synthase (iNOS) activity and subsequently elicits lower level secretions of nitric oxide (NO). However, viability of wild type was unchanged. Taken together, these results indicate that ClpP is involved in the resistance to oxidative stresses after entrapment by macrophages and subsequently contributes to virulence via NO mediated pathway.
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